热休克蛋白70对H2O2诱发大鼠心肌细胞凋亡的保护作用

目的:探讨热休克蛋白70(HSP₇₀)对心肌细胞凋亡的保护作用。方法:体外培养大鼠心肌细胞同时温度诱导细胞产生HSP₇₀,用过氧化氢(H₂O₂)造成心肌细胞损伤。采用免疫组化、DNALadder、流式细胞仪、细胞色素C氧化酶及琥珀酸脱氢酶比活力的测定、电镜观察等作为检测指标的方法。结果:温度诱导后HSP₇₀在胞浆中大量表达,H₂O₂损伤组与HSP₇₀保护组凋亡率(12.18±1.94,6.42±0.86,P<0.01)、细胞色素C氧化酶比活力(5.824±1.949,10.375±2.513)及琥珀酸脱氢酶比活力(0.884±0.152,1.174±0.214,P<0.01)有显著差异。电镜观察损伤组细胞膜、细胞器损伤明显,并出现凋亡小体。结论:HSP₇₀可延迟细胞凋亡,对心肌细胞具有保护作用。

Protective effect of HSP70 on injuried myocardial cells induced by H2O2

AIM: To investigate the role of heat-shock protein 70(HSP_(70)) in the protection of myocardial cells against ischemic injury. METHODS: Myocardial cells were cultured in vitro. HSP_(70) was induced by hyperthermia.H_2O_2-injured myocardial cells were divided into different groups. Flow cytometry, DNA Ladder and biochemistry methods were employed to observe the myocardial cells of different groups. RESULTS: Immunohistochemistry showed hyperthermia induced the up-regulation of HSP_(70) in myocardial cells. Apoptotic rate, activity analysis of cytochrome C and succinic dehydrogenase in H_2O_2-injuried and HSP_(70)-protected groups were obviously different. Electron micrograph shomed hyperthermia alliviated myocardial cell injury induced by H_2O_2. CONCLUSION: HSP_(70) delays apoptosis and protects against H_2O_2-induced myocardial cell injury.