Journal of Hainan Medical University
Volume ,2024 Issue 16
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PANG Jiaoan, YU Yuan, FU Jun, YE Guiyuan, CHEN Weitang, LUO Yanping, TENG Jinhao, LIU Chunli, XIAO Lijun, LI Chengji
2024(16):1201-1209, DOI: 10.13210/j.cnki.jhmu.20240513.001
Abstract:
Objective:To observe the effects of Dahuang Lingxian formula on the expression levels of IKKα， ASK1， MKK3 and CX3CL1 key factors in the MAPK/NF‑κB signaling pathway in the intrahepatic cholangiocyte inflammation model of rats， and to explore the ameliorative effects and possible mechanisms of alleviating intrahepatic cholangiocyte inflammation. Methods:45 SD rats were divided into nine groups according to the complete randomization method， with 5 rats in each group： the blank group， the model group， the Dahuang Lingxian Granules group， the NF‑κB group， the p38MAPK group， the NF‑κB+p38MAPK group， the NF‑κB+Dahuang Lingxian Granules group， the p38MAPK+Dahuang Lingxian Granules group， the NF‑κB+p38MAPK +Dahuang Lingxian Granules group. Except for the blank group， rats in the remaining groups were injected with 5 mg/kg LPS into the common bile duct to prepare an intrahepatic bile duct inflammation model. After the intragastric administration on the 7th day， the rat bile duct tree was removed， and HE staining was used to observe the degree of inflammation. Western blotting and real‑time fluorescence quantitative PCR were used to detect the protein and mRNA expression of IKKα， ASK1， MKK3， and CX3CL1. Results:HE pathology results showed that the inflammation of intrahepatic bile duct tissue and cells in the model group was obvious. After adding Dahuang Lingxian Granules and signal blockers， the inflammation status of intrahepatic bile ducts was improved compared with before， and the difference in total pathological scores was statistically significant （P<0.05）. Compared with the model group， Dahuang Lingxian granules group， p38MAPK group， NF‑κB group， NF‑κB+p38MAPK group， NF‑κB+Dahuang Lingxiang ranules group， p38MAPK+Dahuang Lingxian granules group， NF‑κB+p38MAPK+Dahuang Ling The protein and mRNA expression of ASK1 and CX3CL1 in the Xian Granule group decreased， the expression of MKK3 mRNA increased， and the expression of IKKα in the p38MAPK group and NF‑κB+MKK3 protein in the Dahuang Lingxian Granule group increased （P<0.05）. Compared with the Dahuang Lingxian Granules group，The expression of ASK1 and CX3CL1 mRNA decreased in the p38MAPK group， the NF‑κB group， the NF‑κB+p38MAPK group， the p38MAPK+Dahuang Lingxian Granules group， the NF‑κB+Dahuang Lingxian Granules group， the NF‑κB+p38MAPK+Dahuang Lingxian Granules group. The expression of MKK3 mRNA in the p38MAPK+Dahuang Lingxian Granules group， NF‑κB+Dahuang Lingxian Granules group， and NF‑κB+p38MAPK+Dahuang Lingxian Granules group increased （P<0.05）. Compared with the Dahuang Lingxian Granules group， the IKKα protein expression in the p38MAPK group decreased， and the ASK1 and MKK3 protein expressions in the NF‑κB+Dahuang Lingxian Granules group increased （P<0.05）， while the NF‑κB+p38MAPK+Dahuang Lingxian Granules group increased. The expression of CX3CL1 protein in the granule group decreased（P>0.05）. Conclusion:Dahuang Lingxian Recipe can alleviate the LPS‑induced intrahepatic bile duct inflammatory reaction in rats and promote the repair of bile duct cells， thereby achieving the purpose of reducing the occurrence and postoperative recurrence of PIS. Its mechanism of action may be related to inhibiting the NF‑κB/MAPK signaling pathway. It is related to the activation of key inflammatory factors such as IKKα， ASK1， MKK3 and CX3CL1.
Objective:To observe the effects of Dahuang Lingxian formula on the expression levels of IKKα， ASK1， MKK3 and CX3CL1 key factors in the MAPK/NF‑κB signaling pathway in the intrahepatic cholangiocyte inflammation model of rats， and to explore the ameliorative effects and possible mechanisms of alleviating intrahepatic cholangiocyte inflammation. Methods:45 SD rats were divided into nine groups according to the complete randomization method， with 5 rats in each group： the blank group， the model group， the Dahuang Lingxian Granules group， the NF‑κB group， the p38MAPK group， the NF‑κB+p38MAPK group， the NF‑κB+Dahuang Lingxian Granules group， the p38MAPK+Dahuang Lingxian Granules group， the NF‑κB+p38MAPK +Dahuang Lingxian Granules group. Except for the blank group， rats in the remaining groups were injected with 5 mg/kg LPS into the common bile duct to prepare an intrahepatic bile duct inflammation model. After the intragastric administration on the 7th day， the rat bile duct tree was removed， and HE staining was used to observe the degree of inflammation. Western blotting and real‑time fluorescence quantitative PCR were used to detect the protein and mRNA expression of IKKα， ASK1， MKK3， and CX3CL1. Results:HE pathology results showed that the inflammation of intrahepatic bile duct tissue and cells in the model group was obvious. After adding Dahuang Lingxian Granules and signal blockers， the inflammation status of intrahepatic bile ducts was improved compared with before， and the difference in total pathological scores was statistically significant （P<0.05）. Compared with the model group， Dahuang Lingxian granules group， p38MAPK group， NF‑κB group， NF‑κB+p38MAPK group， NF‑κB+Dahuang Lingxiang ranules group， p38MAPK+Dahuang Lingxian granules group， NF‑κB+p38MAPK+Dahuang Ling The protein and mRNA expression of ASK1 and CX3CL1 in the Xian Granule group decreased， the expression of MKK3 mRNA increased， and the expression of IKKα in the p38MAPK group and NF‑κB+MKK3 protein in the Dahuang Lingxian Granule group increased （P<0.05）. Compared with the Dahuang Lingxian Granules group，The expression of ASK1 and CX3CL1 mRNA decreased in the p38MAPK group， the NF‑κB group， the NF‑κB+p38MAPK group， the p38MAPK+Dahuang Lingxian Granules group， the NF‑κB+Dahuang Lingxian Granules group， the NF‑κB+p38MAPK+Dahuang Lingxian Granules group. The expression of MKK3 mRNA in the p38MAPK+Dahuang Lingxian Granules group， NF‑κB+Dahuang Lingxian Granules group， and NF‑κB+p38MAPK+Dahuang Lingxian Granules group increased （P<0.05）. Compared with the Dahuang Lingxian Granules group， the IKKα protein expression in the p38MAPK group decreased， and the ASK1 and MKK3 protein expressions in the NF‑κB+Dahuang Lingxian Granules group increased （P<0.05）， while the NF‑κB+p38MAPK+Dahuang Lingxian Granules group increased. The expression of CX3CL1 protein in the granule group decreased（P>0.05）. Conclusion:Dahuang Lingxian Recipe can alleviate the LPS‑induced intrahepatic bile duct inflammatory reaction in rats and promote the repair of bile duct cells， thereby achieving the purpose of reducing the occurrence and postoperative recurrence of PIS. Its mechanism of action may be related to inhibiting the NF‑κB/MAPK signaling pathway. It is related to the activation of key inflammatory factors such as IKKα， ASK1， MKK3 and CX3CL1.
2024(16):1210-1219, DOI: 10.13210/j.cnki.jhmu.20240506.004
Abstract:
Objective:To investigate the effect and mechanism of the disassembled prescriptions of Modified Banxia Xiexin Decoction on Helicobacter pylori‑associated gastritis in mice. Methods:Forty SPF‑grade male BALB/c mice were randomly divided into the blank control group（n=6）and the model group（n=34）. The mouse model of Helicobacter pylori associated gastritis with damp‑heat syndrome of spleen and stomach was established and randomly divided into the Modified Banxia Xiexin Decoction group， Qingrezaoshi group， Jianpihewei group，Zaoshixiaopi group and model group， with 6 mice in each group. Each group was given the corresponding drugs by gavage for 4 weeks. The general biological characteristics of mice were observed and recorded； enzyme‑linked immunosorbent assay （ELISA） was used to detect the expression levels of interleukin‑6 （IL‑6）， interleukin‑1β（IL‑1β） and tumor necrosis factor‑α （TNF‑α） in the sera of mice； hematoxylin‑eosin （HE） staining and Giemsa staining were used to observe Hp colonization and pathological changes of the gastric mucosa； quantitative real‑time PCR （qPCR） and immunohistochemistry were used to detect the mRNA and protein expression levels of genes related to the nuclear factor‑κB （NF‑κB） signaling pathway in the gastric mucosa tissues of mice； qPCR was used to detect the contents of Lactobacillus， Bifidobacterium， Enterobacteriaceae， and Enterococcus in the intestinal tracts of mice. Results:Compared with the blank group， the mice in the model group had a decrease in diet and water intake， listlessness， reduced activity， severe gastric mucosal tissue lesions， a large number of Hp colonization， increased serum expression levels of IL‑1β， IL‑6 and TNF‑α （P<0.01）， the mRNA and protein expressions of NF‑κB p65 were up‑regulated （P<0.01）， while the mRNA and protein expressions of IκB‑α were down‑regulated （P<0.01）， the contents of Enterobacteriaceae and Enterococcus were increased （P<0.01）， and the contents of Bifidobacterium and Lactobacillus were decreased （P<0.01）； compared with the model group， the general condition and gastric mucosal lesions of the mice in each treatment group were improved to different degrees， the Hp colonization was reduced， the expression levels of IL‑1β， IL‑6 and TNF‑α in serum were decreased （P<0.05）， the mRNA and protein expressions of NF‑κB p65 were down‑regulated （P<0.05）， and that of IκB‑α were up‑regulated （P<0.05）， and the contents of Enterobacteriaceae and Enterococcus were decreased （P<0.05）， and in the above indexes， the effect was the best in the whole formula group， and the Qingrezaoshi group was better than the Jianpihewei group and Zaoshixiaopi group in the disassembled group， while the content of Bifidobacterium and Lactobacillus was elevated （P<0.05）， and the Jianpihewei group was superior to the Zaoshixiaopigroup and the Qingrezaoshi group. Conclusion:The Modified Banxia Xiexin Decoction can inhibit the colonization of Helicobacter pylori in the gastric mucosa and reduce the damage of the gastric mucosa， which may be related to the inhibition of the inflammatory response mediated by the NF‑κB signaling pathway； and it can promote the growth of intestinal probiotic bacteria while inhibiting the reproduction of harmful bacteria. The Qingrezaoshi group has the best effect in the antibacterial and anti‑inflammatory， and the Jianpihewei group plays a major role in regulating the spleen and stomach， and enhancing human immunity. The whole formula is used to play a synergistic effect of XinKai KuJiang GanBu， which fully reflects the treatment principle of "strengthening healthy Qi and eliminating pathogens， treating both symptoms and root causes" in traditional Chinese medicine.
Objective:To investigate the effect and mechanism of the disassembled prescriptions of Modified Banxia Xiexin Decoction on Helicobacter pylori‑associated gastritis in mice. Methods:Forty SPF‑grade male BALB/c mice were randomly divided into the blank control group（n=6）and the model group（n=34）. The mouse model of Helicobacter pylori associated gastritis with damp‑heat syndrome of spleen and stomach was established and randomly divided into the Modified Banxia Xiexin Decoction group， Qingrezaoshi group， Jianpihewei group，Zaoshixiaopi group and model group， with 6 mice in each group. Each group was given the corresponding drugs by gavage for 4 weeks. The general biological characteristics of mice were observed and recorded； enzyme‑linked immunosorbent assay （ELISA） was used to detect the expression levels of interleukin‑6 （IL‑6）， interleukin‑1β（IL‑1β） and tumor necrosis factor‑α （TNF‑α） in the sera of mice； hematoxylin‑eosin （HE） staining and Giemsa staining were used to observe Hp colonization and pathological changes of the gastric mucosa； quantitative real‑time PCR （qPCR） and immunohistochemistry were used to detect the mRNA and protein expression levels of genes related to the nuclear factor‑κB （NF‑κB） signaling pathway in the gastric mucosa tissues of mice； qPCR was used to detect the contents of Lactobacillus， Bifidobacterium， Enterobacteriaceae， and Enterococcus in the intestinal tracts of mice. Results:Compared with the blank group， the mice in the model group had a decrease in diet and water intake， listlessness， reduced activity， severe gastric mucosal tissue lesions， a large number of Hp colonization， increased serum expression levels of IL‑1β， IL‑6 and TNF‑α （P<0.01）， the mRNA and protein expressions of NF‑κB p65 were up‑regulated （P<0.01）， while the mRNA and protein expressions of IκB‑α were down‑regulated （P<0.01）， the contents of Enterobacteriaceae and Enterococcus were increased （P<0.01）， and the contents of Bifidobacterium and Lactobacillus were decreased （P<0.01）； compared with the model group， the general condition and gastric mucosal lesions of the mice in each treatment group were improved to different degrees， the Hp colonization was reduced， the expression levels of IL‑1β， IL‑6 and TNF‑α in serum were decreased （P<0.05）， the mRNA and protein expressions of NF‑κB p65 were down‑regulated （P<0.05）， and that of IκB‑α were up‑regulated （P<0.05）， and the contents of Enterobacteriaceae and Enterococcus were decreased （P<0.05）， and in the above indexes， the effect was the best in the whole formula group， and the Qingrezaoshi group was better than the Jianpihewei group and Zaoshixiaopi group in the disassembled group， while the content of Bifidobacterium and Lactobacillus was elevated （P<0.05）， and the Jianpihewei group was superior to the Zaoshixiaopigroup and the Qingrezaoshi group. Conclusion:The Modified Banxia Xiexin Decoction can inhibit the colonization of Helicobacter pylori in the gastric mucosa and reduce the damage of the gastric mucosa， which may be related to the inhibition of the inflammatory response mediated by the NF‑κB signaling pathway； and it can promote the growth of intestinal probiotic bacteria while inhibiting the reproduction of harmful bacteria. The Qingrezaoshi group has the best effect in the antibacterial and anti‑inflammatory， and the Jianpihewei group plays a major role in regulating the spleen and stomach， and enhancing human immunity. The whole formula is used to play a synergistic effect of XinKai KuJiang GanBu， which fully reflects the treatment principle of "strengthening healthy Qi and eliminating pathogens， treating both symptoms and root causes" in traditional Chinese medicine.
2024(16):1220-1229, DOI: 10.13210/j.cnki.jhmu.20240429.003
Abstract:
Objective:To explore the potential mechanism of action of Qingjie Huagong decoction（QJHGD） in intervening the intestinal barrier damage in rats with severe acute pancreatitis by using high‑throughput RNA‑Seq. Methods:A SAP model was established by retrograde pancreaticobiliary injection of sodium oxybate， HE was used to observe the histopathological changes in the pancreas and ileum of rats in the blank group， model group and traditional Chinese medicine group， and the levels of serum amylase， lipase， DAO and endotoxin in rats were detected by ELISA method； the differentially expressed genes were detected in ileal tissues of rats in each group by RNA‑seq sequencing， so as to screen the core genes， biological functions and signaling pathways of the QJHGD for intervening in the intestinal barrier damage in rats with severe acute pancreatitis. Results:Compared with the blank group， the pancreas and ileum tissues of rats in the model group showed obvious pathological changes， which were significantly improved by the intervention of QJHGD； the ELISA results suggested that QJHGD could significantly improve the serum amylase， lipase， DAO and endotoxin levels in rats with SAP （P<0.05）.The RNA‑Seq results showed that there were 2 623 genes differentiated in the SAP group from the BG group， and 175 genes were significantly down‑regulated after QJHGD treatment， mainly Tnip3 and Lpo， while 320 genes were up‑regulated， mainly aicda and Tnn， and so on. There were 175 genes whose expression was significantly down‑regulated after QJHGD treatment， mainly Tnip3， Lpo， etc.， while 320 genes were up‑regulated， mainly aicda， Tnn， etc.， which were involved in the regulation of biological processes such as oxidative stress and intervened in multiple signaling pathways such as TJ， apoptosis， Toll‑like receptor， NOD‑like receptor， NF‑κB and so on， and played a role in the regulation of oxidative stress. Conclusion:QJHGD may inhibit the intestinal barrier injury of severe acute pancreatitis by regulating key genes such as Tnip3 and aicda， as well as multiple signaling pathways such as TJ， apoptosis， and Toll‑like receptor.
Objective:To explore the potential mechanism of action of Qingjie Huagong decoction（QJHGD） in intervening the intestinal barrier damage in rats with severe acute pancreatitis by using high‑throughput RNA‑Seq. Methods:A SAP model was established by retrograde pancreaticobiliary injection of sodium oxybate， HE was used to observe the histopathological changes in the pancreas and ileum of rats in the blank group， model group and traditional Chinese medicine group， and the levels of serum amylase， lipase， DAO and endotoxin in rats were detected by ELISA method； the differentially expressed genes were detected in ileal tissues of rats in each group by RNA‑seq sequencing， so as to screen the core genes， biological functions and signaling pathways of the QJHGD for intervening in the intestinal barrier damage in rats with severe acute pancreatitis. Results:Compared with the blank group， the pancreas and ileum tissues of rats in the model group showed obvious pathological changes， which were significantly improved by the intervention of QJHGD； the ELISA results suggested that QJHGD could significantly improve the serum amylase， lipase， DAO and endotoxin levels in rats with SAP （P<0.05）.The RNA‑Seq results showed that there were 2 623 genes differentiated in the SAP group from the BG group， and 175 genes were significantly down‑regulated after QJHGD treatment， mainly Tnip3 and Lpo， while 320 genes were up‑regulated， mainly aicda and Tnn， and so on. There were 175 genes whose expression was significantly down‑regulated after QJHGD treatment， mainly Tnip3， Lpo， etc.， while 320 genes were up‑regulated， mainly aicda， Tnn， etc.， which were involved in the regulation of biological processes such as oxidative stress and intervened in multiple signaling pathways such as TJ， apoptosis， Toll‑like receptor， NOD‑like receptor， NF‑κB and so on， and played a role in the regulation of oxidative stress. Conclusion:QJHGD may inhibit the intestinal barrier injury of severe acute pancreatitis by regulating key genes such as Tnip3 and aicda， as well as multiple signaling pathways such as TJ， apoptosis， and Toll‑like receptor.
SUN Zhao, RAN Binyan, KAN Lina, HUANG Luyu, WU Qiong, WANG Yixiang, KANG Xiaona, LI Dandan, WANG Xiaotong, WANG Xiaolong, JIN Danyang, SHEN Wei
2024(16):1230-1235, DOI: 10.13210/j.cnki.jhmu.20240521.001
Abstract:
Objective:To observe the alterations of brain functional connectivity in the Ventral ttegmental area （VTA） and the Nucleus accumbens （NAcc） in the reward network area of primary patients using functional magnetic resonance imaging （fMRI）. Methods:Twenty-eight patients with primary insomnia were compared with 26 healthy controls， and the relationship between altered functional connectivity in the Ventral Ttegmental Area （VTA） and the Nucleus Accumbens （NAcc） and mood disorders in insomnia was analysed. Results:Comparing primary insomnia patients with healthy controls， the functional connectivity of the VTA and NAcc was reduced in the whole brain. The brain regions with reduced functional connectivity of the VTA-l were bilateral anterior cingulate gyrus and left orbitofrontal gyrus， the brain regions with reduced functional connectivity of the VTA-r were bilateral anterior cingulate gyrus， left orbitofrontal gyrus， and right precentral gyrus， and the brain regions with reduced functional connectivity of the NAcc-l were bilateral thalamus， supplementary motor area， and NAcc-r， and the brain regions with reduced functional connectivity were bilateral thalamus， supplementary motor area， and NAcc-r. The brain regions with reduced NAcc-r functional connectivity were bilateral thalamus and cerebellum. Conclusion:Sleep disorders significantly reduced the functional connectivity between VTA and NAcc in the reward network， suggesting that long-term sleep disorders may affect the reward processing ability of patients with primary insomnia and lead to emotional dysfunction in insomnia patients.
Objective:To observe the alterations of brain functional connectivity in the Ventral ttegmental area （VTA） and the Nucleus accumbens （NAcc） in the reward network area of primary patients using functional magnetic resonance imaging （fMRI）. Methods:Twenty-eight patients with primary insomnia were compared with 26 healthy controls， and the relationship between altered functional connectivity in the Ventral Ttegmental Area （VTA） and the Nucleus Accumbens （NAcc） and mood disorders in insomnia was analysed. Results:Comparing primary insomnia patients with healthy controls， the functional connectivity of the VTA and NAcc was reduced in the whole brain. The brain regions with reduced functional connectivity of the VTA-l were bilateral anterior cingulate gyrus and left orbitofrontal gyrus， the brain regions with reduced functional connectivity of the VTA-r were bilateral anterior cingulate gyrus， left orbitofrontal gyrus， and right precentral gyrus， and the brain regions with reduced functional connectivity of the NAcc-l were bilateral thalamus， supplementary motor area， and NAcc-r， and the brain regions with reduced functional connectivity were bilateral thalamus， supplementary motor area， and NAcc-r. The brain regions with reduced NAcc-r functional connectivity were bilateral thalamus and cerebellum. Conclusion:Sleep disorders significantly reduced the functional connectivity between VTA and NAcc in the reward network， suggesting that long-term sleep disorders may affect the reward processing ability of patients with primary insomnia and lead to emotional dysfunction in insomnia patients.
2024(16):1236-1245, DOI: 10.13210/j.cnki.jhmu.20240510.001
Abstract:
Objective:To investigate the mechanism by which the identity transcription factor （BNC2） of myoblasts targeted by miR‑21‑5p in controling the proliferation， migration， and invasion of esophageal cancer （ESCA） cells. Methods:Real‑time quantitative polymerase chain reaction （qRT‑PCR） was used to assess the relative expression levels of miR‑21‑5P and BNC2 in esophageal cancer tissues. And any differences in expression were statistically analyzed. Following transfection of ECA109 and KYSE30 esophageal cancer cell lines with miR‑21‑5p mimics and miR‑21‑5P inhibitor， and a negative control （NC， including mimcs NC and inhibitor NC）， respectively， the cell function test CCK8，and Transwell was used to investigate the impact of miR‑21‑5p downregulation or overexpression on cell migration， invasion， and proliferation. A bioinformatics technique was utilized to identify and investigate the target genes of miR‑21‑5P. Then， the dual luciferase assay， Western blot， and qRT‑PCR assay were employed to verify the negative regulatory relationship between miR‑21‑5p and the target genes. Result:In ESCA tumor tissues， it was possible to determine that BNC2 had reduced relative expression levels. and the relative expression levels of miR‑21‑5p were greater in tumor tissues by qRT‑PCR detection. The outcomes of the CCK8 and Transwell studies demonstrated that overexpression of miR‑21‑5P increased cell invasion， migration， and proliferation. Cell invasion， migration， and proliferation were all decreased by knocking down miR‑21‑5P. Put differently， miR‑21‑5P functions as an oncogene in esophageal cancers. The bioinformatics technique predicted BNC2 to be the target gene of miR‑21‑5P. According to the results of the dual luciferase assay， miR‑21‑5P was targeted to wild‑type BNC2 '‑UTR. Furthermore， miR‑21‑5p mimics were shown to be able to drastically lower the BNC2 gene level by western blot and qRT‑PCR. On the other hand， a miR‑21‑5p inhibitor may dramatically raise BNC2 expression in esophageal cancer cells. These findings suggest a link of targeting between miR‑21‑5P and BNC2. Conclusion:In ESCA， miR‑21‑5p targets BNC2， and its regulatory role may contribute to cancer proliferation， migration， and invasion.
Objective:To investigate the mechanism by which the identity transcription factor （BNC2） of myoblasts targeted by miR‑21‑5p in controling the proliferation， migration， and invasion of esophageal cancer （ESCA） cells. Methods:Real‑time quantitative polymerase chain reaction （qRT‑PCR） was used to assess the relative expression levels of miR‑21‑5P and BNC2 in esophageal cancer tissues. And any differences in expression were statistically analyzed. Following transfection of ECA109 and KYSE30 esophageal cancer cell lines with miR‑21‑5p mimics and miR‑21‑5P inhibitor， and a negative control （NC， including mimcs NC and inhibitor NC）， respectively， the cell function test CCK8，and Transwell was used to investigate the impact of miR‑21‑5p downregulation or overexpression on cell migration， invasion， and proliferation. A bioinformatics technique was utilized to identify and investigate the target genes of miR‑21‑5P. Then， the dual luciferase assay， Western blot， and qRT‑PCR assay were employed to verify the negative regulatory relationship between miR‑21‑5p and the target genes. Result:In ESCA tumor tissues， it was possible to determine that BNC2 had reduced relative expression levels. and the relative expression levels of miR‑21‑5p were greater in tumor tissues by qRT‑PCR detection. The outcomes of the CCK8 and Transwell studies demonstrated that overexpression of miR‑21‑5P increased cell invasion， migration， and proliferation. Cell invasion， migration， and proliferation were all decreased by knocking down miR‑21‑5P. Put differently， miR‑21‑5P functions as an oncogene in esophageal cancers. The bioinformatics technique predicted BNC2 to be the target gene of miR‑21‑5P. According to the results of the dual luciferase assay， miR‑21‑5P was targeted to wild‑type BNC2 '‑UTR. Furthermore， miR‑21‑5p mimics were shown to be able to drastically lower the BNC2 gene level by western blot and qRT‑PCR. On the other hand， a miR‑21‑5p inhibitor may dramatically raise BNC2 expression in esophageal cancer cells. These findings suggest a link of targeting between miR‑21‑5P and BNC2. Conclusion:In ESCA， miR‑21‑5p targets BNC2， and its regulatory role may contribute to cancer proliferation， migration， and invasion.
2024(16):1246-1258, DOI: 10.13210/j.cnki.jhmu.20240425.001
Abstract:
Objective:To explore the potential target and mechanism of Zhuanggu Zhitong formula in the treatment of postmenopausal osteoporosis. Methods:The PPI network of drug action targets was screened from the BATMAN-TCM database and PMOP disease targets were obtained from GeneCards， TTD， and OMIM databases. This network was then established using the STRING database and visualized with Cytoscape software to create a 'drug-active ingredient-target-disease' network. Additionally， molecular docking was employed to confirm the binding ability between core active components and key targets. Molecular docking technique was used to verify the binding ability of core active components to key targets. The animal model of postmenopausal osteoporosis was established. Mirco-CT and HE staining were used to explore the effect of Zhuanggu Zhitong formula in the treatment of postmenopausal osteoporosis. RT-PCR was used to evaluate the expression of mRNA. Results:69 active ingredient targets and disease common targets of Zhuanggu Zhitong formula were obtained. The key targets of PPI analysis were PPARG， PTGS2， ESR1 and so on. Drug-active ingredient-target-disease network revealed that the core active components were stigmasterol， isopsoralen， ursolic acid， oleanolic acid and so on. The results of molecular docking showed that they had strong binding ability. GO function analysis showed that the main biological function was the response to hormones. The main pathways related to KEGG enrichment were the pathogenesis of cancer， estrogen signal pathway and so on. CT scanning and HE staining can effectively relieve postmenopausal osteoporosis. RT-PCR showed that the expression of PTGS2mRNA was significantly increased and the expression of PPARG was significantly decreased in Zhuanggu Zhitong group. Conclusion:Zhuanggu Zhitong formula can treat PMOP with multi-components， multi-targets and multi-pathways. The main components of Zhuanggu Zhitong formula are stigmasterol， Angelicin， ursolic acid and oleanolic acid. Zhuanggu Zhitong formula acts on human INS， AKT1， PPARG， PTGS2 and ESR1 through metabolic pathway and estrogen signal pathway.
Objective:To explore the potential target and mechanism of Zhuanggu Zhitong formula in the treatment of postmenopausal osteoporosis. Methods:The PPI network of drug action targets was screened from the BATMAN-TCM database and PMOP disease targets were obtained from GeneCards， TTD， and OMIM databases. This network was then established using the STRING database and visualized with Cytoscape software to create a 'drug-active ingredient-target-disease' network. Additionally， molecular docking was employed to confirm the binding ability between core active components and key targets. Molecular docking technique was used to verify the binding ability of core active components to key targets. The animal model of postmenopausal osteoporosis was established. Mirco-CT and HE staining were used to explore the effect of Zhuanggu Zhitong formula in the treatment of postmenopausal osteoporosis. RT-PCR was used to evaluate the expression of mRNA. Results:69 active ingredient targets and disease common targets of Zhuanggu Zhitong formula were obtained. The key targets of PPI analysis were PPARG， PTGS2， ESR1 and so on. Drug-active ingredient-target-disease network revealed that the core active components were stigmasterol， isopsoralen， ursolic acid， oleanolic acid and so on. The results of molecular docking showed that they had strong binding ability. GO function analysis showed that the main biological function was the response to hormones. The main pathways related to KEGG enrichment were the pathogenesis of cancer， estrogen signal pathway and so on. CT scanning and HE staining can effectively relieve postmenopausal osteoporosis. RT-PCR showed that the expression of PTGS2mRNA was significantly increased and the expression of PPARG was significantly decreased in Zhuanggu Zhitong group. Conclusion:Zhuanggu Zhitong formula can treat PMOP with multi-components， multi-targets and multi-pathways. The main components of Zhuanggu Zhitong formula are stigmasterol， Angelicin， ursolic acid and oleanolic acid. Zhuanggu Zhitong formula acts on human INS， AKT1， PPARG， PTGS2 and ESR1 through metabolic pathway and estrogen signal pathway.
2024(16):1259-1265, DOI: 10.13210/j.cnki.jhmu.20231023.004
Abstract:
Objective:To compare the efcacy and safety of Vonoprazan‑Amoxicillin（VA） dual therapy versus proton pump inhibitor （PPI）‑based bismuth‑containing quadruple therapy（BCQ） in the eradication of Helicobacter（H.） pylori. Methods:We performed a systematic search in PubMed， Embase， Cochrane Library，CNKI，and Wanfang databases for relevant clinic trials up to September 2019.The related literatures were analyzed by RevMan 5. 4 software. Results:Eleven studies with 3 033 patients were evaluated in this meta‑analysis. The H.pylori radication rate of VA dual Therapy was compared with PPI‑based quadruple therapy （P>0.05） by intention‑to‑treat （ITT） analysis and per‑protocol（PP） analysis. The incidence of adverse events in VA dual therapy was lower than that in PPI‑based quadruple therapy ［pooled incidence， 11.5% vs. 25.3%， RR： 0.46，95%CI： 0.39~0.54，P<0.001］.Subgroup analysis showed that vonoprazan and high‑dose amoxicillin（VHA） dual therapy had a higher eradication rate than BCQ（ITT pooledincidence，91.8% vs. 82.6%，RR =1.09，95% CI：1.03~1.17，P<0.05；PP pooled incidence，95.6% vs. 86.7%，RR=1.08，95% CI：1.02~1.14，P<0.05）. Conclusions:VA dual therapy can be recommended for H. pylori eradication therapy.
Objective:To compare the efcacy and safety of Vonoprazan‑Amoxicillin（VA） dual therapy versus proton pump inhibitor （PPI）‑based bismuth‑containing quadruple therapy（BCQ） in the eradication of Helicobacter（H.） pylori. Methods:We performed a systematic search in PubMed， Embase， Cochrane Library，CNKI，and Wanfang databases for relevant clinic trials up to September 2019.The related literatures were analyzed by RevMan 5. 4 software. Results:Eleven studies with 3 033 patients were evaluated in this meta‑analysis. The H.pylori radication rate of VA dual Therapy was compared with PPI‑based quadruple therapy （P>0.05） by intention‑to‑treat （ITT） analysis and per‑protocol（PP） analysis. The incidence of adverse events in VA dual therapy was lower than that in PPI‑based quadruple therapy ［pooled incidence， 11.5% vs. 25.3%， RR： 0.46，95%CI： 0.39~0.54，P<0.001］.Subgroup analysis showed that vonoprazan and high‑dose amoxicillin（VHA） dual therapy had a higher eradication rate than BCQ（ITT pooledincidence，91.8% vs. 82.6%，RR =1.09，95% CI：1.03~1.17，P<0.05；PP pooled incidence，95.6% vs. 86.7%，RR=1.08，95% CI：1.02~1.14，P<0.05）. Conclusions:VA dual therapy can be recommended for H. pylori eradication therapy.
2024(16):1266-1270, DOI: 10.13210/j.cnki.jhmu.20240423.001
Abstract:
Prostate cancer is one of the most common cancers in men， and the tumor microenvironment （TME） of prostate cancer patients usually features immunosuppressive properties， including impaired T-cell function， infiltration of immunosuppressive cells， and overexpression of immune checkpoints. Therefore， improvement in the TME is crucial for enhancing the effectiveness of immunotherapy. Therapy plans best suited to individual patients can be determined through immune monitoring， genomic analysis， and assessment of TME characteristics. However， due to significant differences between individual patients， personalized treatment strategies become particularly important. This review delves into the immunotherapy of prostate cancer， especially the intervention and individualized treatment strategies for TME， as well as the multilevel therapeutic combinations. It aims to provide new therapeutic ideas and methods for prostate cancer patients so as to improve their survival rate and quality of life， and to provide a strong theoretical basis for the treatment of this common cancer.
Prostate cancer is one of the most common cancers in men， and the tumor microenvironment （TME） of prostate cancer patients usually features immunosuppressive properties， including impaired T-cell function， infiltration of immunosuppressive cells， and overexpression of immune checkpoints. Therefore， improvement in the TME is crucial for enhancing the effectiveness of immunotherapy. Therapy plans best suited to individual patients can be determined through immune monitoring， genomic analysis， and assessment of TME characteristics. However， due to significant differences between individual patients， personalized treatment strategies become particularly important. This review delves into the immunotherapy of prostate cancer， especially the intervention and individualized treatment strategies for TME， as well as the multilevel therapeutic combinations. It aims to provide new therapeutic ideas and methods for prostate cancer patients so as to improve their survival rate and quality of life， and to provide a strong theoretical basis for the treatment of this common cancer.
2024(16):1271-1275, DOI: 10.13210/j.cnki.jhmu.20240407.003
Abstract:
Diabetes kidney disease （DKD） is a kind of kidney disease characterized by progressive renal tissue fibrosis. On the premise that diabetes is the cause of kidney damage and chronic kidney disease （CKD） caused by other reasons is excluded， type 1 and type 2 diabetes patients can be diagnosed with DKD if they have persistent albuminuria， or if the estimated glomerular filtration rate has declined for more than 3 months， or if renal biopsy conforms to the pathological diagnosis of DKD. The cell communication network （CCN） family of proteins is a group of intercellular matrix proteins involved in regulating important cellular pathophysiological changes such as growth， apoptosis， aging， autophagy， migration， differentiation， and inflammation. Recent studies have shown that the CCN family proteins are significantly upregulated in the DKD rat kidney model， suggesting that they play an important role in the epithelial-mesenchymal transition （EMT） of DKD renal tubular epithelial cells and the progression of renal interstitial fibrosis. This article reviews the role and mechanism of CCN family proteins in mediating renal injury in DKD， in order to explore potential therapeutic targets for DKD.
Diabetes kidney disease （DKD） is a kind of kidney disease characterized by progressive renal tissue fibrosis. On the premise that diabetes is the cause of kidney damage and chronic kidney disease （CKD） caused by other reasons is excluded， type 1 and type 2 diabetes patients can be diagnosed with DKD if they have persistent albuminuria， or if the estimated glomerular filtration rate has declined for more than 3 months， or if renal biopsy conforms to the pathological diagnosis of DKD. The cell communication network （CCN） family of proteins is a group of intercellular matrix proteins involved in regulating important cellular pathophysiological changes such as growth， apoptosis， aging， autophagy， migration， differentiation， and inflammation. Recent studies have shown that the CCN family proteins are significantly upregulated in the DKD rat kidney model， suggesting that they play an important role in the epithelial-mesenchymal transition （EMT） of DKD renal tubular epithelial cells and the progression of renal interstitial fibrosis. This article reviews the role and mechanism of CCN family proteins in mediating renal injury in DKD， in order to explore potential therapeutic targets for DKD.
2024(16):1276-1280, DOI: 10.13210/j.cnki.jhmu.20240305.001
Abstract:
Neuromyelitis optic spectrum disease （NMOSD） is a rare acquired and heterogeneous neuro-ophthalmic crossover disease. It specifically occurs in the central nervous system such as the optic nerve and spinal cord， causing severe disability and blindness. Although the importance of complement in the pathogenesis of NMOSD has been confirmed， the key regulatory role of membrane complement regulatory factor in the pathogenesis of NMOSD is not fully understood. Discussing its physiological and pathological role in the pathogenesis of NMOSD may be one of the important reasons to explain the central pathogenesis of NMOSD. This review focuses on the recent research progress of complement regulatory factors CD46， CD55 and CD59 related to the pathogenesis of NMOSD， and attempts to analyze and review the current status and future development prospects of complement regulatory factors in the pathogenesis of NMOSD.
Neuromyelitis optic spectrum disease （NMOSD） is a rare acquired and heterogeneous neuro-ophthalmic crossover disease. It specifically occurs in the central nervous system such as the optic nerve and spinal cord， causing severe disability and blindness. Although the importance of complement in the pathogenesis of NMOSD has been confirmed， the key regulatory role of membrane complement regulatory factor in the pathogenesis of NMOSD is not fully understood. Discussing its physiological and pathological role in the pathogenesis of NMOSD may be one of the important reasons to explain the central pathogenesis of NMOSD. This review focuses on the recent research progress of complement regulatory factors CD46， CD55 and CD59 related to the pathogenesis of NMOSD， and attempts to analyze and review the current status and future development prospects of complement regulatory factors in the pathogenesis of NMOSD.
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2021,27(13):1036-1040, DOI: 10.13210/j.cnki.jhmu.20200706.001
Abstract:
Hepatic fibrosis is a common pathological basis for all chronic liver diseases， and a necessary stage for the progression of chronic liver disease into cirrhosis. Since various cells and cytokines， as pathogenic factors， play a major role in hepatic fibrosis， the pathogenesis of hepatic fibrosis is extremely complicated. This review focuses on the role of different cells and cytokines （macrophages， natural killer cells and natural killer T cells， tumor necrosis factor， IL-22， transforming growth factor beta， connective tissue growth factor， vascular endothelial growth factor） in the progression of hepatic fibrosis.
Hepatic fibrosis is a common pathological basis for all chronic liver diseases， and a necessary stage for the progression of chronic liver disease into cirrhosis. Since various cells and cytokines， as pathogenic factors， play a major role in hepatic fibrosis， the pathogenesis of hepatic fibrosis is extremely complicated. This review focuses on the role of different cells and cytokines （macrophages， natural killer cells and natural killer T cells， tumor necrosis factor， IL-22， transforming growth factor beta， connective tissue growth factor， vascular endothelial growth factor） in the progression of hepatic fibrosis.
2021,27(17):1350-1354, DOI: 10.13210/j.cnki.jhmu.20200814.002
Abstract:
Cytokines play an important role in the pathological process of atherosclerosis （AS）， affecting the progression and prognosis of AS-related cerebrovascular diseases. Cytokines mainly include C-reactive protein， interleukin， tumor necrosis factor， chemotactic cytokines， matrix metalloproteinases， etc. These cytokines promote or inhibit the inflammatory response and plaque formation during AS process through different targets and mechanisms. A comprehensive understanding of the cytokines in the occurrence and development of AS is conducive to search for new therapeutic targets and drugs.
Cytokines play an important role in the pathological process of atherosclerosis （AS）， affecting the progression and prognosis of AS-related cerebrovascular diseases. Cytokines mainly include C-reactive protein， interleukin， tumor necrosis factor， chemotactic cytokines， matrix metalloproteinases， etc. These cytokines promote or inhibit the inflammatory response and plaque formation during AS process through different targets and mechanisms. A comprehensive understanding of the cytokines in the occurrence and development of AS is conducive to search for new therapeutic targets and drugs.
2024(6):475-480, DOI: 10.13210/j.cnki.jhmu.20230804.003
Abstract:
Hepatocellular carcinoma （HCC） is one of the most common malignant tumors in the world. Its formation is a complex process， and the specific mechanism of its formation hasn't been cleared yet. Due to the fact that most HCC patients are diagnosed in the late stage， and they often lose good surgical opportunities. The emergence of targeted drugs has brought new hope to current HCC patients and can also serve as one of the measures for postoperative treatment， playing a huge role in treating HCC. Sorafenib is the first targeted drug used to treat HCC. It can induce apoptosis of liver tumor cells and inhibit proliferation and angiogenesis of liver tumor cells， so it can improve the survival rate of some patients. However， according to current research， 50% ⁃60% of HCC patients experience a decrease in sensitivity to the drug. It is mainly because Sorafenib will inhibit relevant signaling pathways in vivo after using， which leads to the occurrence of drug resistance， so further exploring the mechanism of Sorafenib resistance and reversing Sorafenib resistance have extremely important clinical value for improving the prognosis of liver cancer treatment. In recent years， many scholars have devoted themselves to studying the close relationship between Sorafenib mediated autophagy and drug resistance through Hippo/YAP and PI3K/Akt/mTOR signaling pathways. And exploring the molecular mechanisms of drug resistance has led to significant development in this field. Therefore， this article mainly discusses the relationship between Hippo/YAP and PI3K/Akt/mTOR signaling pathways and autophagy， as well as the mechanism of drug resistance mediated by them， so as to provide a reliable Scientific theory basis for drug resistance of Sorafenib in the treatment of liver cancer.
Hepatocellular carcinoma （HCC） is one of the most common malignant tumors in the world. Its formation is a complex process， and the specific mechanism of its formation hasn't been cleared yet. Due to the fact that most HCC patients are diagnosed in the late stage， and they often lose good surgical opportunities. The emergence of targeted drugs has brought new hope to current HCC patients and can also serve as one of the measures for postoperative treatment， playing a huge role in treating HCC. Sorafenib is the first targeted drug used to treat HCC. It can induce apoptosis of liver tumor cells and inhibit proliferation and angiogenesis of liver tumor cells， so it can improve the survival rate of some patients. However， according to current research， 50% ⁃60% of HCC patients experience a decrease in sensitivity to the drug. It is mainly because Sorafenib will inhibit relevant signaling pathways in vivo after using， which leads to the occurrence of drug resistance， so further exploring the mechanism of Sorafenib resistance and reversing Sorafenib resistance have extremely important clinical value for improving the prognosis of liver cancer treatment. In recent years， many scholars have devoted themselves to studying the close relationship between Sorafenib mediated autophagy and drug resistance through Hippo/YAP and PI3K/Akt/mTOR signaling pathways. And exploring the molecular mechanisms of drug resistance has led to significant development in this field. Therefore， this article mainly discusses the relationship between Hippo/YAP and PI3K/Akt/mTOR signaling pathways and autophagy， as well as the mechanism of drug resistance mediated by them， so as to provide a reliable Scientific theory basis for drug resistance of Sorafenib in the treatment of liver cancer.
LI Peng?yu, CUI Fu?yan, HUANG Jin?yue, TANG Meng, JIANG Jia?xin, MA Ying, XIA Nian?tong, YANG Bo, WANG Zhi?gang
2023(6):22-27, DOI: 10.13210/j.cnki.jhmu.20230217.001
Abstract:
Objective： A chiral resolution method for enantiomers of two chiral nitrogen⁃containing metabolites R⁃gentiandiol and S⁃gentiandiol of swertiamarin in plasma was developed， and the pharmacokinetics of the metabolites were studied. Methods： The metabolites of swertiamarin in vivo were detected by LC⁃MS/MS using Astec Cyclobond Ⅱ Cyclodextrin column （4.6 mm×100 mm， 5 μm）， gradient elution with acetonitrile⁃water as mobile phase， and monitored by multiple reaction monitoring （MRM） method in positive mode. The ion pairs for quantitative analysis are R⁃gentiandiol （m/z 210.04→192.06）， S⁃gentiandiol （m/z 210.04→192.06） and gentianone （m/z 192.02→162.08）. Results： The linear correlation coefficients of the method developed were greater than 0.999， the precision was less than 7.00%， the recovery was 99.57%⁃102.65 %， and the matrix effect was 90.94%⁃91.34 %. The peak tmax of R⁃gentiandiol and S⁃gentiandiol in rat plasma after oral administration of swertiamarin were （1.63±0.23 h and （1.58 ± 0.21） h， t1/2 was （6.23±0.52） h and （5.46±0.38） h， Cmax was （86.79±20.81） ng/mL and （60.72±18.95） ng/mL， and the AUC0⁃24 were （1 094.58±86.37）） （ng·h）/mL and （724.67±58.38） （ng·h）/mL， respectively. Conclusion： The method was highly sensitive with good accuracy and precision， and it was successfully applied for chiral resolution and pharmacokinetics study of R⁃gentiandiol and S⁃gentiandiol in plasma. The method developed and experimental results will provide scientific basis for the study of pharmacodynamics and pharmacodynamic material basis of swertiamarin， and lay a foundation for clinical application and resource development of TCM monomer.
Objective： A chiral resolution method for enantiomers of two chiral nitrogen⁃containing metabolites R⁃gentiandiol and S⁃gentiandiol of swertiamarin in plasma was developed， and the pharmacokinetics of the metabolites were studied. Methods： The metabolites of swertiamarin in vivo were detected by LC⁃MS/MS using Astec Cyclobond Ⅱ Cyclodextrin column （4.6 mm×100 mm， 5 μm）， gradient elution with acetonitrile⁃water as mobile phase， and monitored by multiple reaction monitoring （MRM） method in positive mode. The ion pairs for quantitative analysis are R⁃gentiandiol （m/z 210.04→192.06）， S⁃gentiandiol （m/z 210.04→192.06） and gentianone （m/z 192.02→162.08）. Results： The linear correlation coefficients of the method developed were greater than 0.999， the precision was less than 7.00%， the recovery was 99.57%⁃102.65 %， and the matrix effect was 90.94%⁃91.34 %. The peak tmax of R⁃gentiandiol and S⁃gentiandiol in rat plasma after oral administration of swertiamarin were （1.63±0.23 h and （1.58 ± 0.21） h， t1/2 was （6.23±0.52） h and （5.46±0.38） h， Cmax was （86.79±20.81） ng/mL and （60.72±18.95） ng/mL， and the AUC0⁃24 were （1 094.58±86.37）） （ng·h）/mL and （724.67±58.38） （ng·h）/mL， respectively. Conclusion： The method was highly sensitive with good accuracy and precision， and it was successfully applied for chiral resolution and pharmacokinetics study of R⁃gentiandiol and S⁃gentiandiol in plasma. The method developed and experimental results will provide scientific basis for the study of pharmacodynamics and pharmacodynamic material basis of swertiamarin， and lay a foundation for clinical application and resource development of TCM monomer.
2021,27(21):1672-1676, DOI: 10.13210/j.cnki.jhmu.20200904.005
Abstract:
Parkinson's disease （PD） is a neurodegenerative disorder due to gradual loss of dopaminergic neurons in the substantia nigra in the midbrain， however， the pathogenesis is unclear. There is a correlation between the excitability of striatal neurons and PD. Ion channels are important to maintain membrane potential and regulate excitability of neurons， but ionic mechanisms for modulation of neurons excitability are not fully understood. This article reviews the relationship between ion channels and excitability of striatal neurons in PD and ion channel changes in the pathogenesis of PD， in order to find new targets to treatment PD by intervening ion channels.
Parkinson's disease （PD） is a neurodegenerative disorder due to gradual loss of dopaminergic neurons in the substantia nigra in the midbrain， however， the pathogenesis is unclear. There is a correlation between the excitability of striatal neurons and PD. Ion channels are important to maintain membrane potential and regulate excitability of neurons， but ionic mechanisms for modulation of neurons excitability are not fully understood. This article reviews the relationship between ion channels and excitability of striatal neurons in PD and ion channel changes in the pathogenesis of PD， in order to find new targets to treatment PD by intervening ion channels.
2023(6):51-61, DOI: 10.13210/j.cnki.jhmu.20210713.001
Abstract:
Objective： To evaluate the clinical efficacy and safety of cinobufagin injection in the treatment of liver cancer. Methods： PubMed database， Embase database and Cochrane Library database， CNKI， Wanfang database， VIP database and Sinomed database were used to search for the randomized controlled trials of cinobufagin injection combined with Western medicine in the treatment of primary liver cancer. The retrieval time was from the establishment to December 15， 2020. Two independent researchers conducted systematic screening， literature inclusion and quality assessment of the articles according to the inclusion criteria， respectively. Meta‑analysis of the data was performed using RevMan 5.4 software. Results： A total of 30 studies with a total of 2 355 patients were included. Compared with conventional western medicine treatment， the clinical effective rate of Hububutin injection combined with western medicine was significantly higher ［RR=1.16，95%CI=（1.11，1.22），P<0.000 01］. It could effectively reduce the tumor size ［RR=1.33，95%CI=（1.17，1.51），P<0.000 01］， prolong the survival time of patients ［RR=1.41，95%CI=（1.31，1.52），P<0.000 01］， improve the quality of life ［RR=1.37，95%CI=（1.19，1.57），P<0.000 01］， improve the liver function of patients ［RR=-14.52，95%CI=（-16.15，-12.88），P<0.000 01］， and reduce the occurrence of adverse reactions ［RR=0.94，95%CI=（0.85，1.42），P=0.25］ such as bone marrow suppression ［RR=0.44，95%CI=（0.31，0.62），P<0.000 01］. Conclusion： Cinobufagin injection combined with western medicine therapy can effectively improve the clinical symptoms of primary liver cancer， and the safety is good. However， the methodological quality of the included literature is low， which affects the objectivity of the outcome， and it still needs to be verified by multi‑sample， multi‑center， randomized double‑blind controlled trial.
Objective： To evaluate the clinical efficacy and safety of cinobufagin injection in the treatment of liver cancer. Methods： PubMed database， Embase database and Cochrane Library database， CNKI， Wanfang database， VIP database and Sinomed database were used to search for the randomized controlled trials of cinobufagin injection combined with Western medicine in the treatment of primary liver cancer. The retrieval time was from the establishment to December 15， 2020. Two independent researchers conducted systematic screening， literature inclusion and quality assessment of the articles according to the inclusion criteria， respectively. Meta‑analysis of the data was performed using RevMan 5.4 software. Results： A total of 30 studies with a total of 2 355 patients were included. Compared with conventional western medicine treatment， the clinical effective rate of Hububutin injection combined with western medicine was significantly higher ［RR=1.16，95%CI=（1.11，1.22），P<0.000 01］. It could effectively reduce the tumor size ［RR=1.33，95%CI=（1.17，1.51），P<0.000 01］， prolong the survival time of patients ［RR=1.41，95%CI=（1.31，1.52），P<0.000 01］， improve the quality of life ［RR=1.37，95%CI=（1.19，1.57），P<0.000 01］， improve the liver function of patients ［RR=-14.52，95%CI=（-16.15，-12.88），P<0.000 01］， and reduce the occurrence of adverse reactions ［RR=0.94，95%CI=（0.85，1.42），P=0.25］ such as bone marrow suppression ［RR=0.44，95%CI=（0.31，0.62），P<0.000 01］. Conclusion： Cinobufagin injection combined with western medicine therapy can effectively improve the clinical symptoms of primary liver cancer， and the safety is good. However， the methodological quality of the included literature is low， which affects the objectivity of the outcome， and it still needs to be verified by multi‑sample， multi‑center， randomized double‑blind controlled trial.
2023(6):1-7, DOI: 10.13210/j.cnki.jhmu.20230106.001
Abstract:
Objective：To explore the establishment of an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells. Methods： SH‑SY5Y cells were randomly divided into control （D‑galactose 0 mmol/L group）， D‑galactose （25 mmol/L， 50 mmol/L， 100 mmol/L， 200 mmol/L， 400 mmol/L） groups， and treated with corresponding concentrations of D‑galactose for 48 h. The changes of cell morphology， β‑galactosidase， the cell morphology， β‑galactosidase activity by microscopic observation， cell proliferation rate by EdU kit and cell survival rate by CCK‑8 assay were used to determine the decaying concentration of D‑galactose and to establish the senescence model. The senescent SH‑SY5Y cells were randomly divided into control group （oxygen glucose deprivation without treatment group）， oxygen glucose deprivation treatment （0.5 h， 1 h， 1.5 h， 2 h） group， followed by re‑glucose reoxygenation for 24 h， and CCK‑8 assay for the survival rate of senescent SH‑SY5Y cells. Results： There were no significant changes in cell morphology and β‑gal activity in the 25 mmol/L and 50 mmol/L groups compared with the control group （P>0.05）， cytosolic hypertrophy was seen in the cells of the 100 mmol/L group， chromatin fixation in the cells of the 200 mmol/L group， and massive vacuolization in the cells of the 400 mmol/L group； the positive rate of β‑galactosidase staining in the cells of the （100-400 mmol/L） group was significantly higher compared with the control group （P< 0.05）， with little difference between the 100 mmol/L and 200 mmol/L groups （P>0.05）； the cell proliferation ability of the （100-400 mmol/L） group was significantly decreased in a concentration‑dependent manner （P<0.05）； the cell survival rate was decreased in a concentration‑dependent manner （P<0.05）， with IC50 between 100 mmol/L and 200 mmol/L. The survival of senescent SH‑SY5Y cells showed a time‑dependent decrease in oxygen‑glucose deprivation （P<0.05）， with an IC50 close to 1 h. Conclusion： D‑gal concentration of 100 mmoL/L and 48 h of cell action could establish a survival rate of about 50% of senescent SH‑SY5Y cells， and oxygen glucose deprivation of senescent SH‑SY5Y cells for 1 h and reperfusion for 24 h could establish an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells with a survival rate close to 50%.
Objective：To explore the establishment of an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells. Methods： SH‑SY5Y cells were randomly divided into control （D‑galactose 0 mmol/L group）， D‑galactose （25 mmol/L， 50 mmol/L， 100 mmol/L， 200 mmol/L， 400 mmol/L） groups， and treated with corresponding concentrations of D‑galactose for 48 h. The changes of cell morphology， β‑galactosidase， the cell morphology， β‑galactosidase activity by microscopic observation， cell proliferation rate by EdU kit and cell survival rate by CCK‑8 assay were used to determine the decaying concentration of D‑galactose and to establish the senescence model. The senescent SH‑SY5Y cells were randomly divided into control group （oxygen glucose deprivation without treatment group）， oxygen glucose deprivation treatment （0.5 h， 1 h， 1.5 h， 2 h） group， followed by re‑glucose reoxygenation for 24 h， and CCK‑8 assay for the survival rate of senescent SH‑SY5Y cells. Results： There were no significant changes in cell morphology and β‑gal activity in the 25 mmol/L and 50 mmol/L groups compared with the control group （P>0.05）， cytosolic hypertrophy was seen in the cells of the 100 mmol/L group， chromatin fixation in the cells of the 200 mmol/L group， and massive vacuolization in the cells of the 400 mmol/L group； the positive rate of β‑galactosidase staining in the cells of the （100-400 mmol/L） group was significantly higher compared with the control group （P< 0.05）， with little difference between the 100 mmol/L and 200 mmol/L groups （P>0.05）； the cell proliferation ability of the （100-400 mmol/L） group was significantly decreased in a concentration‑dependent manner （P<0.05）； the cell survival rate was decreased in a concentration‑dependent manner （P<0.05）， with IC50 between 100 mmol/L and 200 mmol/L. The survival of senescent SH‑SY5Y cells showed a time‑dependent decrease in oxygen‑glucose deprivation （P<0.05）， with an IC50 close to 1 h. Conclusion： D‑gal concentration of 100 mmoL/L and 48 h of cell action could establish a survival rate of about 50% of senescent SH‑SY5Y cells， and oxygen glucose deprivation of senescent SH‑SY5Y cells for 1 h and reperfusion for 24 h could establish an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells with a survival rate close to 50%.
WEI Wu?jun, WANG Chun?fang, JIANG Qi, XU Gui?dan, HUANG Jing?jing, LIN Cheng, HU Ren?tong, CHANG Zheng?yi
2023(6):8-14, DOI: 10.13210/j.cnki.jhmu.20221221.001
Abstract:
Objective： To investigate the effect of mir⁃3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells， and to verify its target gene. Methods： The expression of mir⁃3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR， and mir⁃3168 mimic， inhibitor and negative control were synthesized. They were transfected into AGS and AGS/DDP gastric cancer cells， respectively. The expression of mir⁃3168 and TP53 mRNA was detected by qPCR. Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment， apoptosis was detected by flow cytometry， cell invasion was detected by Transwell， and TP53 protein expression was detected by western blot， The database predicted the binding sites of mir⁃3168 and TP53. According to the binding sites， the double luciferase experiment was used to verify the binding of mir⁃3168 and TP53. Results： Compared with cisplatin sensitive gastric cancer cell AGS， mir⁃3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP； mir⁃3168 mimic promotes cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 inhibitor inhibits cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and promotes apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 mimic inhibits the expression of TP53 mRNA and protein， and mir⁃3168 inhibitor promotes the expression of TP53 mRNA and protein； Targetscan database predicted that there was a binding point between mir⁃3168 and TP53， and the double luciferase experiment suggested that mir⁃3168 was bound to TP53 through the predicted binding site. Conclusion： mir⁃3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.
Objective： To investigate the effect of mir⁃3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells， and to verify its target gene. Methods： The expression of mir⁃3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR， and mir⁃3168 mimic， inhibitor and negative control were synthesized. They were transfected into AGS and AGS/DDP gastric cancer cells， respectively. The expression of mir⁃3168 and TP53 mRNA was detected by qPCR. Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment， apoptosis was detected by flow cytometry， cell invasion was detected by Transwell， and TP53 protein expression was detected by western blot， The database predicted the binding sites of mir⁃3168 and TP53. According to the binding sites， the double luciferase experiment was used to verify the binding of mir⁃3168 and TP53. Results： Compared with cisplatin sensitive gastric cancer cell AGS， mir⁃3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP； mir⁃3168 mimic promotes cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 inhibitor inhibits cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and promotes apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 mimic inhibits the expression of TP53 mRNA and protein， and mir⁃3168 inhibitor promotes the expression of TP53 mRNA and protein； Targetscan database predicted that there was a binding point between mir⁃3168 and TP53， and the double luciferase experiment suggested that mir⁃3168 was bound to TP53 through the predicted binding site. Conclusion： mir⁃3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.
2023(6):15-21, DOI: 10.13210/j.cnki.jhmu.20211221.002
Abstract:
Objective： To investigate whether "Fuzheng Qingretonglin" decoction can reduce urinary tract damage caused by complex urinary tract infection caused by drug resistant Escherichia coli by regulating Nod‑like receptor pyrin domain3 inflammasome， and to explore the feasibility of this decoction combined with levofloxacin in the treatment of complex urinary tract infection caused by drug resistant bacteria. Methods： SD rats were divided into five groups： sham group， model group， levofloxacin group（Lev group）， levofloxacin+Fuzheng Qingre Tonglin decoction group（FZ+lev group）， and Fuzheng Qingre Tonglin decoction group（FZQRTL group）. After the experiment， urine was taken for bacterial culture to determine the urinary tract infection of rats in each group； HE staining was used to observe the pathological changes of kidney and bladder tissues in rats； The expression of NLRP3 in kidney and bladder tissues was detected by immunohistochemistry； The expression of IL‑1β and IL‑18 in serum of rats was detected by ELISA； The expressions of NLRP3，ASC and Caspase‑1 were detected by Western blotting. Results： The positive rate of urine bacteria culture in the sham group was 0%， the positive rate of urine bacteria culture in the model group was 100%； and the positive rate of urine bacteria culture in the FZ+lev group was 37.50%， which was statistically different from that in the model group（P<0.05）. A large number of inflammatory cells were observed in the kidney and bladder tissues of the model group by HE staining， while the number of inflammatory cells in the kidney and bladder tissues of the Lev group and FZQRTL group was significantly reduced compared with that of the model group. The FZ+lev group in the number and structure of inflammatory cells in kidney and bladder were similar to the sham group. The NLRP3 immunohistochemistry of kidney and bladder tissue in FZ+lev groups and FZQRTL groups was significantly different from that in model group（P<0.001）. The levels of IL‑1β and IL‑18 in serum of Lev group，FZQRTL group and FZ+lev group were significantly decreased by ELISA compared with model group（P<0.001）. The levels of IL‑1β and IL‑18 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. The protein expressions of NLRP3， ASC and Caspase‑1 in the Lev group， FZQRTL group and FZ+lev group were significantly lower than those in the model group（P<0.001）. The protein expressions of NLRP3， ASC and Caspase‑1 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. Conclusion： "Fuzheng Qingretonglin" decoction may have a protective effect on the kidney and bladder of rats with complex urinary tract infection caused by drug‑resistant Escherichia coli by inhibiting the activation of NLRP3 inflammatory bodies， and TCM combined with levofloxacin has a better therapeutic effect than TCM or levofloxacin alone.
Objective： To investigate whether "Fuzheng Qingretonglin" decoction can reduce urinary tract damage caused by complex urinary tract infection caused by drug resistant Escherichia coli by regulating Nod‑like receptor pyrin domain3 inflammasome， and to explore the feasibility of this decoction combined with levofloxacin in the treatment of complex urinary tract infection caused by drug resistant bacteria. Methods： SD rats were divided into five groups： sham group， model group， levofloxacin group（Lev group）， levofloxacin+Fuzheng Qingre Tonglin decoction group（FZ+lev group）， and Fuzheng Qingre Tonglin decoction group（FZQRTL group）. After the experiment， urine was taken for bacterial culture to determine the urinary tract infection of rats in each group； HE staining was used to observe the pathological changes of kidney and bladder tissues in rats； The expression of NLRP3 in kidney and bladder tissues was detected by immunohistochemistry； The expression of IL‑1β and IL‑18 in serum of rats was detected by ELISA； The expressions of NLRP3，ASC and Caspase‑1 were detected by Western blotting. Results： The positive rate of urine bacteria culture in the sham group was 0%， the positive rate of urine bacteria culture in the model group was 100%； and the positive rate of urine bacteria culture in the FZ+lev group was 37.50%， which was statistically different from that in the model group（P<0.05）. A large number of inflammatory cells were observed in the kidney and bladder tissues of the model group by HE staining， while the number of inflammatory cells in the kidney and bladder tissues of the Lev group and FZQRTL group was significantly reduced compared with that of the model group. The FZ+lev group in the number and structure of inflammatory cells in kidney and bladder were similar to the sham group. The NLRP3 immunohistochemistry of kidney and bladder tissue in FZ+lev groups and FZQRTL groups was significantly different from that in model group（P<0.001）. The levels of IL‑1β and IL‑18 in serum of Lev group，FZQRTL group and FZ+lev group were significantly decreased by ELISA compared with model group（P<0.001）. The levels of IL‑1β and IL‑18 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. The protein expressions of NLRP3， ASC and Caspase‑1 in the Lev group， FZQRTL group and FZ+lev group were significantly lower than those in the model group（P<0.001）. The protein expressions of NLRP3， ASC and Caspase‑1 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. Conclusion： "Fuzheng Qingretonglin" decoction may have a protective effect on the kidney and bladder of rats with complex urinary tract infection caused by drug‑resistant Escherichia coli by inhibiting the activation of NLRP3 inflammatory bodies， and TCM combined with levofloxacin has a better therapeutic effect than TCM or levofloxacin alone.
CHEN Huan?xiong, HE Xian?bo, LI Guo?jun, TANG Song?jie, ZHONG Zhen?hao，, HUANG Tao, LIN You?cai, LIN Su?yu, MENG Zhi?bin
2023(6):43-50, DOI: 10.13210/j.cnki.jhmu.20230116.001
Abstract:
Objective： To study the position and the grade of screw perforation in the apical region of adolescent idiopathic scoliosis （AIS） surgery using a calibration technique for the intraoperative navigation error， and to analyze the related factors of navigation deviation and the clinical significance of the calibration technique. Methods： From 2017 to 2020， a total of 60 Lenke 1 AIS surgical cases were enrolled in this research. The 30 cases received surgery using the intraoperative navigation system （Navigation group） and another 30 cases were assisted with intraoperative navigation system with calibration technique （Calibration group） for the intraoperative navigation error. The basic information and radiological data of the both groups were all recorded. According to the Fu Chang⁃feng’s pedicle channel classification system， the pedicle on the apical region of the two groups was classified. And then the accuracy of screw placement of the two groups was evaluated according to the Rao’s classification. Results： A total of 600 screws were placed in the two groups. The 297 and 303 pedicle screws were implanted in the navigation group and the calibration group， respectively. In the apical region of the calibration group， the rates of the grade 0 screw placement in type A， B and C pedicle were 95.7%， 86.7% and 68.9% respectively. It was a statistically significant difference from the 73.9%， 66.9% and 30.0% in the navigation group respectively （P<0.05）. In the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 1.6%， 1.6% and 0%， respectively. The corresponding rates were 16.3%， 16.9%， 30.0% and 47.6% in the navigation group， respectively. Moreover， in the concave side of the apical region of the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 3.6%， 2.6% and 0%， respectively. Compared with the calibration group， the corresponding rates were higher in the navigation group （34.4%， 25.9%， 37.2% and 60.0%， respectively）. No serious complications such as spinal cord or neurovascular injury occurred for the two groups. Conclusion： Compared with the intraoperative navigation system， the calibration technique for the intraoperative navigation error could provide the higher accuracy of pedicle screw placement in the apical region of the major curve， the lower medial cortical perforation rate， the less screws misplacement rate on the concave side and the less complication rate of the severe Lenke 1 AIS patients.
Objective： To study the position and the grade of screw perforation in the apical region of adolescent idiopathic scoliosis （AIS） surgery using a calibration technique for the intraoperative navigation error， and to analyze the related factors of navigation deviation and the clinical significance of the calibration technique. Methods： From 2017 to 2020， a total of 60 Lenke 1 AIS surgical cases were enrolled in this research. The 30 cases received surgery using the intraoperative navigation system （Navigation group） and another 30 cases were assisted with intraoperative navigation system with calibration technique （Calibration group） for the intraoperative navigation error. The basic information and radiological data of the both groups were all recorded. According to the Fu Chang⁃feng’s pedicle channel classification system， the pedicle on the apical region of the two groups was classified. And then the accuracy of screw placement of the two groups was evaluated according to the Rao’s classification. Results： A total of 600 screws were placed in the two groups. The 297 and 303 pedicle screws were implanted in the navigation group and the calibration group， respectively. In the apical region of the calibration group， the rates of the grade 0 screw placement in type A， B and C pedicle were 95.7%， 86.7% and 68.9% respectively. It was a statistically significant difference from the 73.9%， 66.9% and 30.0% in the navigation group respectively （P<0.05）. In the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 1.6%， 1.6% and 0%， respectively. The corresponding rates were 16.3%， 16.9%， 30.0% and 47.6% in the navigation group， respectively. Moreover， in the concave side of the apical region of the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 3.6%， 2.6% and 0%， respectively. Compared with the calibration group， the corresponding rates were higher in the navigation group （34.4%， 25.9%， 37.2% and 60.0%， respectively）. No serious complications such as spinal cord or neurovascular injury occurred for the two groups. Conclusion： Compared with the intraoperative navigation system， the calibration technique for the intraoperative navigation error could provide the higher accuracy of pedicle screw placement in the apical region of the major curve， the lower medial cortical perforation rate， the less screws misplacement rate on the concave side and the less complication rate of the severe Lenke 1 AIS patients.
YAN Dong?ming, LIANG Jian?tang, LIU Xiao?qian, LI Meng?yongwei, DING Shun, MENG Qing?wen, ZHANG Si?yuan, TANG Cai?ying, LIU Qi?bing, YANG Kun
2023(6):28-36, DOI: 10.13210/j.cnki.jhmu.20221125.001
Abstract:
Objective： To investigate the prognostic value of ORMDL2 in human glioma and its relationship with immune invasion. Methods： The clinical survival data from TCGA – LGG&GBM， CGGA and GEO were used to evaluate the clinical prognostic value of ORMDL2. The cut off value of ORMDL2 was detected with pROC package to draw ROC curve to prove its value in differential diagnosis of glioma. The first 300 genes with the most significant positive correlation with ORMDL2 were selected to establish PPI network through STRING database and conduct GO and pathway analysis. The relationship between the expression of ORMDL2 mRNA and immune cell infiltration was investigated by using ssGSEA and TIMER2.0 databases. Results： The expression of ORMDL2 mRNA in glioma was significantly higher than that in adjacent normal tissues， and the difference was most significant in high‑grade glioma. The expression of ORMDL2 was increased in human glioma， which was related to the clinicopathological characteristics and poor prognosis of glioma patients. In addition， the increased expression of ORMDL2 was associated with a series of immune infiltrating cells， including macrophages. Conclusion： ORMDL2 plays an important role in glioma immune cell infiltration and is a biomarker of prognosis of glioma patients.
Objective： To investigate the prognostic value of ORMDL2 in human glioma and its relationship with immune invasion. Methods： The clinical survival data from TCGA – LGG&GBM， CGGA and GEO were used to evaluate the clinical prognostic value of ORMDL2. The cut off value of ORMDL2 was detected with pROC package to draw ROC curve to prove its value in differential diagnosis of glioma. The first 300 genes with the most significant positive correlation with ORMDL2 were selected to establish PPI network through STRING database and conduct GO and pathway analysis. The relationship between the expression of ORMDL2 mRNA and immune cell infiltration was investigated by using ssGSEA and TIMER2.0 databases. Results： The expression of ORMDL2 mRNA in glioma was significantly higher than that in adjacent normal tissues， and the difference was most significant in high‑grade glioma. The expression of ORMDL2 was increased in human glioma， which was related to the clinicopathological characteristics and poor prognosis of glioma patients. In addition， the increased expression of ORMDL2 was associated with a series of immune infiltrating cells， including macrophages. Conclusion： ORMDL2 plays an important role in glioma immune cell infiltration and is a biomarker of prognosis of glioma patients.
Abstract:
Objective: To study the effect of Baihe Dihuang Decoction in improving anxiety and its mechanism of action. Methods: Male mice were randomly divided into 5 groups: blank control group, Baihe Dihuang Decoction high, medium, low-dose group and diazepam group. After continuous intragastric administration for 14 d, the behavioral test of the mouse elevated plus maze experiment and opening test was performed. The brain tissue GABA and Glu content was measured by immunosorbent assay (ELISA). Results: Compared with the blank control group, the middle and high doses of Baihe Dihuang Decoction could increase the time and frequency of movement of the mice in the open cross labyrinth in the open arm and increase the number of times that the mouse entered the central area in the opening test. The anti-anxiety effect also showed an increase in the brain tissue GABA content in mice, ignificantly decreased Glu contents in mice. Conclusion: Baihe Dihuang Decoction has some anxiolytic effect, and antianxiety effect may be related to increasing brain tissue GABA content, decreased Glu contents in mice.
Objective: To study the effect of Baihe Dihuang Decoction in improving anxiety and its mechanism of action. Methods: Male mice were randomly divided into 5 groups: blank control group, Baihe Dihuang Decoction high, medium, low-dose group and diazepam group. After continuous intragastric administration for 14 d, the behavioral test of the mouse elevated plus maze experiment and opening test was performed. The brain tissue GABA and Glu content was measured by immunosorbent assay (ELISA). Results: Compared with the blank control group, the middle and high doses of Baihe Dihuang Decoction could increase the time and frequency of movement of the mice in the open cross labyrinth in the open arm and increase the number of times that the mouse entered the central area in the opening test. The anti-anxiety effect also showed an increase in the brain tissue GABA content in mice, ignificantly decreased Glu contents in mice. Conclusion: Baihe Dihuang Decoction has some anxiolytic effect, and antianxiety effect may be related to increasing brain tissue GABA content, decreased Glu contents in mice.
2021,27(7):555-560, DOI: 10.13210/j.cnki.jhmu.20200930.003
Abstract:
Ulcerative colitis （UC） is a type of chronic inflammatory recurrent disease. The etiology and pathogenesis are still unclear by now. Among them， immune factors are usually considered to be the final link in the pathogenesis of UC. Due to the increasing incidence， long course of the disease， and difficult recovery， the relevant research is gradually deepened， and related research on intestinal flora， immunity， genetics， etc. has become a hot spot. A large amount of evidence indicates that regulatory T cells （Treg）， helper T cells 17 （Th17）， Th17/Treg immune axis and intestinal microbiota in UC patients play an important role in regulating the development of diseases. There is also a certain correlation between the bacterial flora and the Th17/Treg immune axis. Therefore， this article examines Th17/Treg cells， intestinal microbiota and the relationship between them by consulting a large number of relevant data at home and abroad in recent years. The formation of the immune axis and other issues are briefly summarized， with a view to providing more practical basis for clinical targeted therapy.
Ulcerative colitis （UC） is a type of chronic inflammatory recurrent disease. The etiology and pathogenesis are still unclear by now. Among them， immune factors are usually considered to be the final link in the pathogenesis of UC. Due to the increasing incidence， long course of the disease， and difficult recovery， the relevant research is gradually deepened， and related research on intestinal flora， immunity， genetics， etc. has become a hot spot. A large amount of evidence indicates that regulatory T cells （Treg）， helper T cells 17 （Th17）， Th17/Treg immune axis and intestinal microbiota in UC patients play an important role in regulating the development of diseases. There is also a certain correlation between the bacterial flora and the Th17/Treg immune axis. Therefore， this article examines Th17/Treg cells， intestinal microbiota and the relationship between them by consulting a large number of relevant data at home and abroad in recent years. The formation of the immune axis and other issues are briefly summarized， with a view to providing more practical basis for clinical targeted therapy.
2023(6):73-78, DOI: 10.13210/j.cnki.jhmu.20210701.001
Abstract:
Coronary no‑reflow phenomenon belongs to a type of coronary microcirculation disturbance， and its main pathogenic factors are vascular endothelial cell injury， microembolism and inflammatory reaction， which are corresponding to the pathogenesis of choroid injury， blood stasis and heat toxin in traditional Chinese medicine， such as NO， ET‑1， chemokine， IL and other cytokines. The degree of improvement of patients' symptoms and laboratory examination data provide a basis for traditional Chinese medicine compound prescription， monomer and traditional Chinese medicine characteristic therapy for the treatment of no-reflow phenomena（NRP）. Combined with related factors， the author summarizes the research progress of traditional Chinese medicine treatment of NRP in recent years， in order to provide clinical reference.
Coronary no‑reflow phenomenon belongs to a type of coronary microcirculation disturbance， and its main pathogenic factors are vascular endothelial cell injury， microembolism and inflammatory reaction， which are corresponding to the pathogenesis of choroid injury， blood stasis and heat toxin in traditional Chinese medicine， such as NO， ET‑1， chemokine， IL and other cytokines. The degree of improvement of patients' symptoms and laboratory examination data provide a basis for traditional Chinese medicine compound prescription， monomer and traditional Chinese medicine characteristic therapy for the treatment of no-reflow phenomena（NRP）. Combined with related factors， the author summarizes the research progress of traditional Chinese medicine treatment of NRP in recent years， in order to provide clinical reference.
Abstract:
Objective: The current study aims to identify the effects of exogenous application of pulsed electromagnetic fields on skin wound healing in diabetic rats, and thus provides experimental evidence for its more scientific clinical application in the future. Methods: The diabetic animal models were established via intraperitoneal injection of streptozotocin in 4-monthold male rats. Fourth eight rats were randomly assigned into the diabetes group (DM) and diabetes coupled with pulsed electromagnetic fields (DM+PEMF) group. Another 24 normal rats were used as the blank control group (Control). Then, all the rats in the three groups were subjected to dorsal surgery for the establishment of soft tissue wound model (circular wound with the diameter of 2 cm). Then, the rats in the DM+PEMF group were subjected to pulsed electromagnetic fields stimulation. Then, 6 rats in each group were sacrificed at Day 5, 12 and 19 post surgery. The glucose levels, wound closure, wound healing time and tissue tensile strength were examined and analyzed. Results: Pulsed electromagnetic fields significantly increased the wound closure rate in diabetic rats at Day 5, 12 and 19 post surgery, decreased overall wound healing period in diabetic rats, and also enhanced tissue tensile strength in diabetic rats at Day 5, 12 and 19 post surgery. Conclusion: Low-intensity pulsed electromagnetic fields can significantly accelerate diabetic wound healing process, and also improve diabetic tissue repair capacity. This study may be helpful for providing more scientific and reasonable experimental evidence for the treatment of pulsed electromagnetic fields on diabetic wound healing in clinics.
Objective: The current study aims to identify the effects of exogenous application of pulsed electromagnetic fields on skin wound healing in diabetic rats, and thus provides experimental evidence for its more scientific clinical application in the future. Methods: The diabetic animal models were established via intraperitoneal injection of streptozotocin in 4-monthold male rats. Fourth eight rats were randomly assigned into the diabetes group (DM) and diabetes coupled with pulsed electromagnetic fields (DM+PEMF) group. Another 24 normal rats were used as the blank control group (Control). Then, all the rats in the three groups were subjected to dorsal surgery for the establishment of soft tissue wound model (circular wound with the diameter of 2 cm). Then, the rats in the DM+PEMF group were subjected to pulsed electromagnetic fields stimulation. Then, 6 rats in each group were sacrificed at Day 5, 12 and 19 post surgery. The glucose levels, wound closure, wound healing time and tissue tensile strength were examined and analyzed. Results: Pulsed electromagnetic fields significantly increased the wound closure rate in diabetic rats at Day 5, 12 and 19 post surgery, decreased overall wound healing period in diabetic rats, and also enhanced tissue tensile strength in diabetic rats at Day 5, 12 and 19 post surgery. Conclusion: Low-intensity pulsed electromagnetic fields can significantly accelerate diabetic wound healing process, and also improve diabetic tissue repair capacity. This study may be helpful for providing more scientific and reasonable experimental evidence for the treatment of pulsed electromagnetic fields on diabetic wound healing in clinics.
The mechanism and application of specialized phagocytic cell burial function in chronic wound repair
2024(13):1035-1040, DOI: 10.13210/j.cnki.jhmu.20240005.001
Abstract:
Chronic wounds， as a long‑term wasting disease， are a long‑term clinical problem that is difficult to solve. Dysfunction of efferocytosis prevents apoptotic cells from being cleared from the wound in time， resulting in secondary cell necrosis and release of pro‑inflammatory cytokines， making it difficult for the wound to transition from the inflammatory phase to the proliferative phase. Macrophages and dendritic cells， as professional phagocytes， are the main bearers of efferocytosis. This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis‑related receptors， macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM‑1， NK‑4， MIR‑21， CD36， etc.， to accelerate the healing of chronic wounds. In addition， the efferocytosis function of dendritic cells may be limited by SLC7A11. Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing. This study is of great significance to further elucidating the healing process of chronic refractory wound and the development of new treatmentss.
Chronic wounds， as a long‑term wasting disease， are a long‑term clinical problem that is difficult to solve. Dysfunction of efferocytosis prevents apoptotic cells from being cleared from the wound in time， resulting in secondary cell necrosis and release of pro‑inflammatory cytokines， making it difficult for the wound to transition from the inflammatory phase to the proliferative phase. Macrophages and dendritic cells， as professional phagocytes， are the main bearers of efferocytosis. This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis‑related receptors， macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM‑1， NK‑4， MIR‑21， CD36， etc.， to accelerate the healing of chronic wounds. In addition， the efferocytosis function of dendritic cells may be limited by SLC7A11. Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing. This study is of great significance to further elucidating the healing process of chronic refractory wound and the development of new treatmentss.
2023(6):68-72, DOI: 10.13210/j.cnki.jhmu.20210310.001
Abstract:
The occurrence of cardiovascular events is one of the important causes of death and disability in the nation. The ischemia and hypoxia of myocardial cells caused by coronary atherosclerosis， intravascular stenosis or myocardial infarction leads to cell damage， necrosis and apoptosis， leading to Myocardial fibrosis affects cardiac function and the quality of life of patients. Reducing myocardial cell apoptosis， inhibiting myocardial fibrosis and promoting myocardial cell regeneration are of great significance for maintaining the normal shape and function of the heart. With the progress of research， scientists have discovered that the Hippo pathway plays an important role in the repair and regeneration of myocardial cells. This article reviews the regulatory effects and mechanisms of the various factors in the Hioop signaling pathway in the repair and regeneration of cardiomyocytes.
The occurrence of cardiovascular events is one of the important causes of death and disability in the nation. The ischemia and hypoxia of myocardial cells caused by coronary atherosclerosis， intravascular stenosis or myocardial infarction leads to cell damage， necrosis and apoptosis， leading to Myocardial fibrosis affects cardiac function and the quality of life of patients. Reducing myocardial cell apoptosis， inhibiting myocardial fibrosis and promoting myocardial cell regeneration are of great significance for maintaining the normal shape and function of the heart. With the progress of research， scientists have discovered that the Hippo pathway plays an important role in the repair and regeneration of myocardial cells. This article reviews the regulatory effects and mechanisms of the various factors in the Hioop signaling pathway in the repair and regeneration of cardiomyocytes.
2021,27(17):1281-1284, DOI: 10.13210/j.cnki.jhmu.20210716.002
Abstract:
The outbreak of COVID‑19 caused by severe acute respiratory syndrome coronavirus type 2 （SARS‑CoV‑2） in 2019 threatens global public health. In the early stage， respiratory symptoms are the most common in patients with new coronal pneumonia， but with the spread of the disease around the world， gastrointestinal symptoms such as diarrhea， nausea and vomiting have attracted more and more attention. And some patients take diarrhea as the first symptom， which is easy to cause missed diagnosis. This paper expounds the close relationship between COVID‑19 and gastrointestinal tract， and reviews the research progress of COVID‑19's effect on gastrointestinal tract.
The outbreak of COVID‑19 caused by severe acute respiratory syndrome coronavirus type 2 （SARS‑CoV‑2） in 2019 threatens global public health. In the early stage， respiratory symptoms are the most common in patients with new coronal pneumonia， but with the spread of the disease around the world， gastrointestinal symptoms such as diarrhea， nausea and vomiting have attracted more and more attention. And some patients take diarrhea as the first symptom， which is easy to cause missed diagnosis. This paper expounds the close relationship between COVID‑19 and gastrointestinal tract， and reviews the research progress of COVID‑19's effect on gastrointestinal tract.
CHEN Ze?shan, WEN Bin, ZHU Wen?lin, DENG Xin, PENG Pei?chun, JIAN Ruo?han, LAN Hong?ni, CHEN Bo?yao, LV Yan, LIANG Xin?qiu
2023(6):62-67, DOI: 10.13210/j.cnki.jhmu.20210824.009
Abstract:
microRNA（miRNA） is a type of single‑stranded small molecule non‑coding RNA that interacts with the 3'untranslated region of the target gene to achieve negative regulation of the target gene and participate in multiple links of cell proliferation and apoptosis. At present， there is evidence that miRNA‑155 is involved in the occurrence and development of a variety of liver diseases. By consulting relevant literature reports， this article summarizes the effects of miRNA‑155 in non‑alcoholic fatty liver disease， alcoholic liver disease， viral hepatitis， acute liver failure， and liver disease. The research progress of fibrosis and liver cancer in a variety of liver diseases， and the potential of miRNA‑155 as a non‑invasive biomarker is analyzed to provide a reference for exploring the diagnosis and treatment of liver diseases.
microRNA（miRNA） is a type of single‑stranded small molecule non‑coding RNA that interacts with the 3'untranslated region of the target gene to achieve negative regulation of the target gene and participate in multiple links of cell proliferation and apoptosis. At present， there is evidence that miRNA‑155 is involved in the occurrence and development of a variety of liver diseases. By consulting relevant literature reports， this article summarizes the effects of miRNA‑155 in non‑alcoholic fatty liver disease， alcoholic liver disease， viral hepatitis， acute liver failure， and liver disease. The research progress of fibrosis and liver cancer in a variety of liver diseases， and the potential of miRNA‑155 as a non‑invasive biomarker is analyzed to provide a reference for exploring the diagnosis and treatment of liver diseases.
2021,27(11):872-875, DOI: 10.13210/j.cnki.jhmu.20200714.001
Abstract:
Drug resistance is a major problem when using molecular targeted drugs for tumors. Currently， functional gene screening is the most common strategy for screening drug resistance genes. In recent years， CRISPR‑Cas9 gene‑editing technology has been widely used in functional studies on tumor‑related genes because of its high accuracy， simplicity， and efficiency. In this paper， the principle of CRISPR‑Cas9 library screening technology and its application in functional gene screening are reviewed. At the same time， the application prospect of the CRISPR‑Cas9 technology is forecasted.
Drug resistance is a major problem when using molecular targeted drugs for tumors. Currently， functional gene screening is the most common strategy for screening drug resistance genes. In recent years， CRISPR‑Cas9 gene‑editing technology has been widely used in functional studies on tumor‑related genes because of its high accuracy， simplicity， and efficiency. In this paper， the principle of CRISPR‑Cas9 library screening technology and its application in functional gene screening are reviewed. At the same time， the application prospect of the CRISPR‑Cas9 technology is forecasted.
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