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目的探讨丙泊酚预处理对大鼠离体心肌缺氧再给氧损伤时心肌细胞凋亡及线粒体细胞色素C释放的影响。方法50只SD大鼠随机分为5组:对照组(C组),DMSO预处理组(D组),25、50、100μmol.L-1丙泊酚预处理组(P1、P2、P3组)。应用Langendorff离体心脏灌注模型,经主动脉用K-H液逆行灌注。各组均缺氧30min,再给氧60min。DMSO组、P1、P2、P3组在缺氧前分别以含DMSO、相应浓度丙泊酚的K-H液灌注10min,再冲洗5min,重复2次。记录平衡灌注末、缺氧前即刻、再给氧30、60min时的心功能指标。再给氧60min时用DNA原位末端缺口标记技术(TUNEL法)测定凋亡细胞,提取心肌线粒体,免疫印迹法测定线粒体和胞质的细胞色素C水平。结果D组与C组相比差异无显著性;与D组相比,P1、P2、P3组再给氧30min、60min时LVEDP降低、LVDP升高(P<0.05),再给氧末心肌细胞凋亡率降低(P<0.05或0.01),心肌线粒体细胞色素C释放减少,胞质细胞色素C的量明显降低(P<0.05或0.01)。结论丙泊酚预处理能够通过抑制心肌线粒体细胞色素C释放到胞质降低心肌细胞凋亡率,减轻心肌缺氧再给氧损伤。
Objective To investigate the effects of propofol preconditioning on cardiomyocyte apoptosis and mitochondrial cytochrome C release in isolated rat myocardium during anoxia-reoxygenation injury. Methods Fifty SD rats were randomly divided into 5 groups: control group (C), DMSO pretreatment group (D), 25, 50 and 100μmol.L-1 propofol preconditioning group ). The Langendorff model of isolated heart perfusion was performed retrogradely with K-H fluid via the aorta. Each group was hypoxia 30min, then oxygen for 60min. DMSO group, P1, P2 and P3 groups were pretreated with K-H solution containing DMSO and propofol respectively for 10 min and then for 5 min before hypoxia. Balance at the end of perfusion records, hypoxia immediately, and then oxygen 30,60min cardiac function. Apoptotic cells were detected by DNA in situ nick nick labeling (TUNEL) method at 60 min of oxygen supply. Myocardial mitochondria were extracted and the level of cytochrome C in mitochondria and cytoplasm was determined by immunoblotting. Results There was no significant difference between group D and group C. Compared with group D, group P1, P2 and P3 were reoxygenated for 30 min, LVEDP decreased and LVDP increased at 60 min (P <0.05) Apoptosis rate decreased (P <0.05 or 0.01), mitochondrial cytochrome C release decreased, the amount of cytoplasmic cytochrome C decreased significantly (P <0.05 or 0.01). CONCLUSION: Propofol preconditioning can reduce myocardial apoptosis rate and inhibit myocardial oxygen deficit reoxygenation by inhibiting the release of mitochondrial cytochrome c into the cytoplasm.