| The delivery of oxygen and nutriments and wastes in myocardium is the basis of normal working of hearts. If the blood supply of hearts decreases or the hearts overrun, myocardium will be injured because of relative or absolute ischemia. By the experiments and clinical studies, we observed blood stream resuming after brief ischemia caused myocardium injuried worse because of ischemia-reperfusion injury of myocardium. It is urgent necessary to search a safe and effective new drug to prevent ischemia-reperfusion injury of myocardium from Chinese traditional medicines. In this study, we want to investigate the validity and the cellular and molecular mechanism of Ginsenoside Re preventing ischemia-reperfusion injury of myocardium by models of wistar rats of ischemia-reperfusion injury of myocardium in vivo and models of myocardium injuried in vitro.1. The study of protective effect and mechanism of Ginsenoside Re on myocardial cells in vitro:The wistar rats are taked as experimental animal. In our study, the oxygen and and nutriments in myocardial cells in vitro wered breaked off three hours, then recoverd for one hour. By this model, the morphologic change of myocardial cells wered observed. The myocardial cells swelled, shrank and fell off, the beating of myocardial cells was not normal, butGinsenoside Re can lighten these changes. The myocardial cells survival rates in model group decreased, compared with normal group the difference was significant, but the growth of myocardial cells was very well in Ginsenoside Re group. The release of LDH in model group was much more than in normal group, while the release of LDH in Ginsenoside Re group was restrained. The vigor of Na-K-ATP enzyme and Ca2+-ATP enzyme of myocardial cells in model group was much lower than that in normal group and Ginsenoside Re can increase the vigor of Na-K-ATP enzyme and Ca2+-ATP enzyme. The flow cytometry analysis showed that the apoptosis rate of myocardial cells in model group was higher than that in normal group and the ratio of myocardial cells in Go/G1 period increased and the ratio of cells in G2/M and S period decreased, while Ginsenoside Re can decreased the apoptosis rate of myocardial cells. The flurorescence microscope observation showed that there were many apoptosis and necrosis myocardial cells in model group, but there was little apoptosis and necrosis cells in normal group.2.The study of protective effects of Ginsenoside Re on rat myocardium of ischemia-reperfusion injury:The model of ischemia-reperfusion injury of rat myocardium in vivo were induced by the ligation of left coronary artery and the effect of blood stream dynamics of rat myocardium of Re on ischemia-reperfusion injury were observed. In ischemia-reperfusion group the heart rate decreased, at the same time the SBP, DBP, MAP, LVSP anddp/dtmax all decreased obviously. In much dose group the LVSP,眃p/dtmax, SBP, DBP and MAP increased obviously, and in little dose group LVSP, +dp/dtmas and SBP increased. The blood viscosity and plasma viscosity all increased obviously. We also observed the effect of Ginsenoside Re on enzymes of rat myocardium of ischemia-reperfusion injury. The expression of AST, LDH and CK-MB in ischemia-reperfusion group increased obviously, while therelease of AST, LDH and CK-MB in Re group reduced. The observation of the histological changes showed that the rat myocardium was normal in control group and the shape of nucleus of myocardium cells was abnormal in ischemia-reperfusion group, some myocardium cells swelled, but in Re group these changes were very little. The detection of electron-microscopy were that in ischemia-reperfusion group the stroma and the mitochondria swelled and vacuoles appeared in nucleus, nucleus were larger, the membrane of nucleus broadened, chromatin condensed and apoptotic bodies came into being. Ginsenoside Re can reduce the range of myocardial infarction.3.The molecular mechanism of protective effects of Ginsenoside Re on rat myocardium of ischemia-reperfusion injury:We observed the...
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