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目的观察二氮嗪对缺血-再灌流心肌细胞凋亡,以及对Bax、Bcl-2和Caspase-3表达的影响。方法21只SD大鼠随机分为假手术组(sham operation,SO),缺血-再灌流组(ischemia/reperfusion,IR)和二氮嗪处理组(Diazoxide,DI)。SO组和IR组静脉注射相应量溶媒,DI组12.5 mg/kg剂量静脉注射二氮嗪。10min后SO组不结扎前降支,4 h后取心脏,而IR组和DI组结扎前降支2 h,再灌流2 h。采用TUNEL法和免疫组化法检测缺血心肌细胞凋亡和Bax、Bcl-2、Caspase-3表达,及心肌梗死范围。结果与SO组相比,IR和DI组心肌细胞凋亡率显著增加(P<0.05),Bax、Bcl-2和Caspase-3蛋白阳性细胞指数明显升高(P<0.05);与IR组相比,DI组明显降低心肌细胞凋亡率(P<0.05)和Bax,Caspase-3蛋白阳性细胞指数(P<0.05),增加Bcl-2蛋白阳性细胞指数(P<0.05)。IR组心肌梗死范围为(36.9±2.3)%,DI组为(20.0±8)%,两组差异有显著性(P<0.05)。结论二氮嗪通过上调Bcl-2表达,下调Bax及Caspase-3表达而减少在体大鼠缺血-再灌流损伤心肌细胞凋亡。
Objective To observe the effects of diazoxide on cardiomyocyte apoptosis and the expression of Bax, Bcl-2 and Caspase-3 in ischemia-reperfusion myocardium. Methods Twenty-one SD rats were randomly divided into sham operation (SO), ischemia / reperfusion (IR) and Diazoxide (DI) groups. The SO and IR groups received the same amount of intravenous injection of vehicle, while the DI group received intravenous diazoxide at a dose of 12.5 mg / kg. After 10 minutes, the descending branch of SO group was not ligated and the heart was taken after 4 hours. The descending branch of IR group and DI group were ligated for 2 hours and reperfused for 2 hours. TUNEL and immunohistochemistry were used to detect the expression of Bax, Bcl-2 and Caspase-3 in ischemic myocardium and the extent of myocardial infarction. Results Compared with SO group, the apoptotic rates of cardiomyocytes in IR and DI groups were significantly increased (P <0.05), while the positive cells of Bax, Bcl-2 and Caspase-3 were significantly increased (P <0.05) Compared with DI group, the apoptotic rate of cardiomyocytes was significantly decreased (P <0.05), Bax and Caspase-3 protein positive cells index (P <0.05), and Bcl-2 protein positive cells index increased significantly (P <0.05). The range of myocardial infarction was (36.9 ± 2.3)% in IR group and (20.0 ± 8)% in DI group, with significant difference between the two groups (P <0.05). Conclusion Diazoxide can reduce the apoptosis of myocardial cells after ischemia-reperfusion injury in vivo by up-regulating Bcl-2 expression and down-regulating Bax and Caspase-3 expression.