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目的 探讨HSP70对活性氧所致心肌细胞急性损伤的保护作用。方法 用热休克预处理诱导新生大鼠心肌细胞中HSP70的表达 ,采用HSP70反义寡核苷酸阻断HSP70的表达 ,乳酸脱氢酶释放率和细胞总蛋白质合成能力来反映H2 O2 0 .5mM所致心肌细胞损伤程度。结果 H2 O2 引起心肌细胞乳酸脱氢酶释放率明显升高 ,而细胞总蛋白质的合成降低。热休克预处理导致心肌细胞中HSP70表达明显增加 ,并使H2 O2 所致心肌细胞LDH释放率显著降低 ,细胞总蛋白质的合成基本恢复正常水平。HSP70反义寡核苷酸很大程度上阻断了HSP70的表达及热休克预处理的心肌细胞保护作用。结论 在热休克预处理减轻过氧化氢所致乳鼠心肌细胞急性损伤的作用中 ,HSP70发挥了最主要的作用。
Objective To investigate the protective effect of HSP70 on cardiomyocyte acute injury induced by reactive oxygen species. Methods Heat shock preconditioning induced the expression of HSP70 in neonatal rat cardiomyocytes. HSP70 antisense oligonucleotide was used to block the expression of HSP70, the release rate of lactate dehydrogenase and the total protein synthesis ability of the cells to reflect the H2 O2 0.5mM Caused by myocardial injury. Results H2O2 induced a significant increase of lactate dehydrogenase release rate in cardiomyocytes and a decrease in total cellular protein synthesis. Heat shock preconditioning resulted in a significant increase of HSP70 expression in cardiomyocytes, and a significant decrease of LDH release rate in cardiomyocytes induced by H2O2. The total cellular protein synthesis returned to normal levels. HSP70 antisense oligonucleotides blocked the expression of HSP70 and cardiomyocyte protective effect of heat shock preconditioning to a great extent. Conclusion HSP70 plays the most important role in the role of heat shock preconditioning in reducing the acute injury of cardiomyocytes induced by hydrogen peroxide in neonatal rats.