Studies On Influence Of Ginsenoside-Re On Myocardium Ischemia-Reperfusion Injury And Apoptosis Pathway Of Mitochondrial

Myocardial ischemia reperfusion injury (MIRI) refers that reperfusion aggravates functional and structural injury of myocardial ischemic area after temporal ischemia,.Growing evidence from animal experiments and clinical observations proves the phenomenon. And the studies on MIRI becomes a focus in recent years.it is meaningfull to search for a safe and effective drug to improve MIRI from Chinese Ttraditional Medicines.In this study ,We have evaluated the protective efficacy of Ginsenoside Re and researched the cellular and molecular mechanisms of Ginsenoside Re on inhibition of cardiomyocyte apoptosis in MIRI by models of Wistar rats in vivo.Method: Left anterior descending coronary artery was occluded(ischemia) for 30min and reperfused for 4 hours with or without Ginenoside Re, We detected the inflammatory cytokines of TNF-αand IL-1βwith RIA; and myocardial infarct size ;Observed histological changes by HE staining ,and change of ultrastructure of myocardial cells with electron-microscopy; Counted apoptosis index of myocardial cells in ischemic area by TUNEL method with light-microscopy, Analyzed protein expression of caspase-3,9 with immunohistochemical method .Result: Ginsenoside Re decresaed inflammentory cytokines of TNF-αand IL1-βsignificantly;and reduced the range of myocardial infarction ; The observation of the pathomorphology changes showed that the myocardial tissue was normal in control group, and in ischemia-reperfusion group part of myocardium was necrosis or d egeneration ,some cytoplasmic of myocardial cell was swelling, some nucleus were deeply stained, Inflammatory cell infiltrated in stram, but in Re group these changes were very little. The detection of electron-microscopy were that in ischemia reperfusion group the mitochondria swelled and increased, chromatin condensed at the edge of nuclear membrane, and apoptotic bodies came into being, the membrane of nucleus broadened, nucleus were larger and vacuoles appeared in it; The apoptosis index was (42.32±8.76)% in ischemia reperfusion group,and (31.66±5.65)% in low-dose Re treated group (30.55±7.35) % in high-dose Re treated group; Protein expression of caspase-3 and caspase-9 were increased significantly in the ischemia reperfusion group and Re treated group when compared with the control group(P<0.01), there was significant different in the expression of caspase-3 and caspase-9 between Re treated group and ischemia reperfusion group(P<0.05).Conclusions: Ginsenoside Re can decrease inflammentory factors of TNF-αand IL1-β; lighten myocardium injury; inhibit cardiomyocyte apoptosis; reduce protein expression of caspase-3 and caspase-9 . It is conclude that Ginsenoside Re reduces the injured myocardium of ischemia-reperfusion in vivo and inhibits cardiomyocyte apoptosis by reducing protein expression of caspase-3 and caspase-9.