Wenxin Liu, Xintao Deng, Yamin Su, Haihua Geng, Min Pan
{"title":"绞股蓝皂苷对心肌缺血再灌注损伤的影响及其机制。","authors":"Wenxin Liu, Xintao Deng, Yamin Su, Haihua Geng, Min Pan","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>The present study aimed to clarify the effects of Gypenosides on myocardial ischemia-reperfusion injury. Using rat H9c2 cardiomyocytes as the research object, the model of cardiomyocyte hypoxia and reoxygenation was established to observe the protective effects of Gypenosides on myocardial ischemia-reperfusion injury, revealing the key targets and possible mechanisms for Gypenosides to exert myocardial protection.</p><p><strong>Material and methods: </strong>A model of cardiomyocyte hypoxia and reoxygenation was prepared. The activity of cardiomyocytes was detected by CCK-8 method. The cardiomyocyte injury was evaluated by LDH assay. The cardiomyocyte apoptosis rate was detected by flow cytometry. The mitochondrial membrane potential of cardiomyocytes was detected by JC-1 staining. Western blot was used to detect the expression of MPTP downstream apoptotic pathways and MPTP opening-related regulatory factors.</p><p><strong>Results: </strong>The cell survival rate of each Gypenosides pretreatment group was significantly higher than that of the hypoxia-reoxygenation group, indicating that Gypenosides could inhibit cell apoptosis and the decrease of mitochondrial membrane potential of hypoxia-reoxygenation cells. The expressions Cytochrome C, APAFl, Caspase-9, and Caspase-3 proteins were significantly lower than those of the hypoxia-reoxygenation group, the expression of Bax was significantly lower than those of the hypoxia-reoxygenation group, while the expression of Bcl2 was significantly higher than those of the hypoxia-reoxygenation group.</p><p><strong>Conclusion: </strong>Gypenosides can effectively reduce myocardial ischemia-reperfusion injury in rats. By regulating Bax and Bcl2, Gypenosides can inhibit MPTP opening and the activation of downstream apoptotic pathways, thereby reducing myocardial ischemia-reperfusion injury.</p>","PeriodicalId":19098,"journal":{"name":"Neuro endocrinology letters","volume":"42 1","pages":"22-27"},"PeriodicalIF":0.6000,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effect of Gypenosides on Myocardial Ischemia- Reperfusion Injury and its Mechanism.\",\"authors\":\"Wenxin Liu, Xintao Deng, Yamin Su, Haihua Geng, Min Pan\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>The present study aimed to clarify the effects of Gypenosides on myocardial ischemia-reperfusion injury. Using rat H9c2 cardiomyocytes as the research object, the model of cardiomyocyte hypoxia and reoxygenation was established to observe the protective effects of Gypenosides on myocardial ischemia-reperfusion injury, revealing the key targets and possible mechanisms for Gypenosides to exert myocardial protection.</p><p><strong>Material and methods: </strong>A model of cardiomyocyte hypoxia and reoxygenation was prepared. The activity of cardiomyocytes was detected by CCK-8 method. The cardiomyocyte injury was evaluated by LDH assay. The cardiomyocyte apoptosis rate was detected by flow cytometry. The mitochondrial membrane potential of cardiomyocytes was detected by JC-1 staining. Western blot was used to detect the expression of MPTP downstream apoptotic pathways and MPTP opening-related regulatory factors.</p><p><strong>Results: </strong>The cell survival rate of each Gypenosides pretreatment group was significantly higher than that of the hypoxia-reoxygenation group, indicating that Gypenosides could inhibit cell apoptosis and the decrease of mitochondrial membrane potential of hypoxia-reoxygenation cells. The expressions Cytochrome C, APAFl, Caspase-9, and Caspase-3 proteins were significantly lower than those of the hypoxia-reoxygenation group, the expression of Bax was significantly lower than those of the hypoxia-reoxygenation group, while the expression of Bcl2 was significantly higher than those of the hypoxia-reoxygenation group.</p><p><strong>Conclusion: </strong>Gypenosides can effectively reduce myocardial ischemia-reperfusion injury in rats. By regulating Bax and Bcl2, Gypenosides can inhibit MPTP opening and the activation of downstream apoptotic pathways, thereby reducing myocardial ischemia-reperfusion injury.</p>\",\"PeriodicalId\":19098,\"journal\":{\"name\":\"Neuro endocrinology letters\",\"volume\":\"42 1\",\"pages\":\"22-27\"},\"PeriodicalIF\":0.6000,\"publicationDate\":\"2021-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuro endocrinology letters\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuro endocrinology letters","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Effect of Gypenosides on Myocardial Ischemia- Reperfusion Injury and its Mechanism.
Objectives: The present study aimed to clarify the effects of Gypenosides on myocardial ischemia-reperfusion injury. Using rat H9c2 cardiomyocytes as the research object, the model of cardiomyocyte hypoxia and reoxygenation was established to observe the protective effects of Gypenosides on myocardial ischemia-reperfusion injury, revealing the key targets and possible mechanisms for Gypenosides to exert myocardial protection.
Material and methods: A model of cardiomyocyte hypoxia and reoxygenation was prepared. The activity of cardiomyocytes was detected by CCK-8 method. The cardiomyocyte injury was evaluated by LDH assay. The cardiomyocyte apoptosis rate was detected by flow cytometry. The mitochondrial membrane potential of cardiomyocytes was detected by JC-1 staining. Western blot was used to detect the expression of MPTP downstream apoptotic pathways and MPTP opening-related regulatory factors.
Results: The cell survival rate of each Gypenosides pretreatment group was significantly higher than that of the hypoxia-reoxygenation group, indicating that Gypenosides could inhibit cell apoptosis and the decrease of mitochondrial membrane potential of hypoxia-reoxygenation cells. The expressions Cytochrome C, APAFl, Caspase-9, and Caspase-3 proteins were significantly lower than those of the hypoxia-reoxygenation group, the expression of Bax was significantly lower than those of the hypoxia-reoxygenation group, while the expression of Bcl2 was significantly higher than those of the hypoxia-reoxygenation group.
Conclusion: Gypenosides can effectively reduce myocardial ischemia-reperfusion injury in rats. By regulating Bax and Bcl2, Gypenosides can inhibit MPTP opening and the activation of downstream apoptotic pathways, thereby reducing myocardial ischemia-reperfusion injury.
期刊介绍：
Neuroendocrinology Letters is an international, peer-reviewed interdisciplinary journal covering the fields of Neuroendocrinology, Neuroscience, Neurophysiology, Neuropsychopharmacology, Psychoneuroimmunology, Reproductive Medicine, Chronobiology, Human Ethology and related fields for RAPID publication of Original Papers, Review Articles, State-of-the-art, Clinical Reports and other contributions from all the fields covered by Neuroendocrinology
Letters.
Papers from both basic research (methodology, molecular and cellular biology, anatomy, histology, biology, embryology, teratology, normal and pathological physiology, biophysics, pharmacology, pathology and experimental pathology, biochemistry, neurochemistry, enzymology, chronobiology, receptor studies, endocrinology, immunology and neuroimmunology, animal physiology, animal breeding and ethology, human ethology, psychology and others) and from clinical research (neurology, psychiatry and child psychiatry, obstetrics and gynecology, pediatrics, endocrinology, immunology, cardiovascular studies, internal medicine, oncology and others) will be considered.
The Journal publishes Original papers and Review Articles. Brief reports, Special Communications, proved they are based on adequate experimental evidence, Clinical Studies, Case Reports, Commentaries, Discussions, Letters to the Editor (correspondence column), Book Reviews, Congress Reports and other categories of articles (philosophy, art, social issues, medical and health policies, biomedical history, etc.) will be taken under consideration.
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