脂微球前列腺素E1对大鼠离体心肌缺血／再灌注损伤的保护作用和机制

目的观察脂微球前列腺素E1（凯时）对大鼠离体心肌缺血/再灌注损伤的保护作用并探讨其可能机制。方法Wistar大鼠24只,随机分成正常对照组、缺血/再灌注损伤组和凯时保护组。利用Langendorff灌流装置复制大鼠心肌缺血/再灌注损伤模型。观察指标：冠状动脉流出液中乳酸脱氢酶（LDH）活性,心肌匀浆中超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量,心肌超微结构,HE染色,TUNEL染色及免疫组化等。结果凯时（10μg/L）可使心肌缺血/再灌注损伤所致的LDH释放显著降低,心肌超微结构损伤减轻,SOD活性升高,MDA含量降低;同时使细胞凋亡减少,Bcl-2表达增加,Bax和Caspase-3表达减少。结论凯时能显著减轻大鼠心肌缺血/再灌注损伤,其机制可能与凯时具有抗氧化、清除自由基和抗细胞凋亡的作用有关。

Protective effect of Lipo-prostaglandin E1 (PGE1) on myocardial ischemia/reperfusion injury in isolated rats

Objective To investigate the protective effect of Lipo-prostaglandin E1（PGE1） on myocardial ischemia/ reperfusion（I/R） injury in isolated heart of rat and its possible mechanism.Methods Twenty-four Wistar rats were randomly divided into 3 groups：control group,I/R group,and PGE1 group.Cardiac I/R injury in isolated heart was duplicated by using Langendorff system.The observed indexes were LDH activity in coronary effluent,SOD and MDA in myocardial homogenate,cardiac ultrastructure and HE dyeing,TUNEL dyeing and immunohistochemistry etc.Results PGE1（10 μg/L） significantly decreased the elevation of LDH activities induced by I/R injury,attenuated cardiac ultrastructural damage,increased SOD activity and decreased MDA contents.Meanwhile it decreased cellular apoptosis,increased Bcl-2 expression,diminished Bax and Caspase-3 expression.Conclusions PGE1 can attenuate markedly the myocardial I/R injury.It＇s mechanism may be related to its role of antioxidation,scavenging free radical and anti- apoptosis.