摘要
目的 观察热应激预适应对H2 O2 诱发乳鼠心肌细胞损伤的保护作用。方法 用胰蛋白酶消化法分离Wistar大鼠乳鼠心肌细胞 ,将其分为正常对照组 (37℃无H2 O2 损伤 ) ,H2 O2 损伤组 (37℃H2 O2 损伤 )和热应激组(4 2℃H2 O2 损伤 )。测定 3组细胞线粒体的琥珀酸脱氢酶 (SDH)比活力、细胞色素C氧化酶 (CCO)比活力 ;应用免疫组化技术检测热休克蛋白 70 (HSP70 )的表达。结果 与正常对照组比较 ,H2 O2 损伤组的SDH、CCO比活力显著下降 (P <0 .0 5 ) ;而热应激组下降不明显 (P >0 .0 5 )。并且 ,HSP70仅在热应激组中大量表达。结论 H2 O2 能够引起乳鼠心肌细胞损伤 ;而热应激预适应对其具有保护作用 。
Objective To observe the protection of heat stress preconditioning on the isolated cardiomyocytes injured by H 2O 2 in rat.Methods Rat cardiomyocytes were cultured with trypsin digestion method and divided into three groups: control group,injured group by H 2O 2 and heat stress group. The activity of succinic dehydrogenase (SDH),cytochrome C oxidase(CCO)were assayed. Meanwhile,heat shock protein 70(HSP70) expression was tested by immunohistochemistry in different groups. Results Compared with the control group, the activity of SDH and CCO in the injured group decreased significantly ( P <0.05),whereas, in the heat stress group it decreased insignificantly( P >0.05). In addition,HSP70 was expressed highly in the heat stress group only. Conclusion The myocardial cells can be injured by H 2O 2. The heat stress preconditioning is able to protect the myocardial cells from being injured by H 2O 2 in rats. It is suggested that the mechanism may be related to highly expression of the HSP70 in the heat stress.
出处
《哈尔滨医科大学学报》
CAS
2003年第1期28-30,共3页
Journal of Harbin Medical University
