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目的观察丙泊酚对离体大鼠心肌缺血再灌注(I-R)损伤的影响,并从线粒体过氧化损伤方面探讨其可能的作用机制。方法应用Langendorff离体心脏灌流系统,全心停灌25 min,再灌注30 min建立心肌I-R损伤模型。记录各项心功能指标;测定心肌线粒体呼吸链的完整性、膜肿胀度和丙二醛(MDA)含量;流式细胞术检测心肌细胞凋亡率及Bcl-2和Bax蛋白的表达,免疫组化法测定半胱氨酸天冬氨酸蛋白酶(caspase)-3,-9和-8的表达。结果与I-R组相比,缺血前10 min开始,并于再灌注期间持续灌流丙泊酚30和60μmol·L~(-1)能明显改善I- R后的心功能;心肌线粒体呼吸链损伤有所恢复,膜肿胀度减轻,MDA生成明显减少,心肌细胞凋亡率明显降低,Bcl-2表达增加,Bax表达减少,caspase-3和caspase-9阳性细胞数明显减少。结论丙泊酚减轻I-R所致的心肌线粒体过氧化损伤,抑制线粒体途径的细胞凋亡,可能是其心肌保护作用机制之
Objective To investigate the effect of propofol on myocardial ischemia-reperfusion (I-R) injury in vitro and to explore its possible mechanism from mitochondrial peroxidation injury. Methods Myocardial I-R injury model was established by Langendorff perfusion cardioplegia system with 25 min perfusion and 30 min reperfusion. The indexes of cardiac function were recorded. The integrity of mitochondrial respiratory chain, membrane swelling and the content of malondialdehyde (MDA) were measured. The apoptosis rate and the expression of Bcl-2 and Bax protein were detected by flow cytometry. Methods The caspase-3, -9, and -8 expressions were determined by the chemiluminescence assay. Results Compared with the IR group, pre-ischemia 10 min and sustained perfusion of 30 and 60 μmol·L -1 propofol during reperfusion could significantly improve the cardiac function after I-R; myocardial mitochondrial respiratory chain injury After recovery, the swelling of the membrane was reduced, the MDA production was significantly reduced, the apoptosis rate of cardiomyocytes was significantly decreased, the expression of Bcl-2 was increased, the expression of Bax was decreased, and the number of caspase-3 and caspase-9 positive cells was significantly decreased. Conclusions Propofol can reduce myocardial mitochondrial peroxisative damage induced by I-R and inhibit the mitochondrial pathway of apoptosis, which may be the mechanism of myocardial protection