热休克预处理抗过氧化氢所致心肌细胞损伤保护作用的细胞分子机理  

^Protective effect of heat shock pretreatment on cardioznyocytes against bydrogen peroxide induced injury and its molecular mechanism

作　　者：肖献忠[1] 王燕如[1] 刘梅冬[1] 罗正曜[1] 

机构地区：[1]湖南医科大学病理生理学教研室

出　　处：《中国病理生理杂志》1997年第1期65-69,共5页Chinese Journal of Pathophysiology

摘　　要：体外培养的鸡胚心肌细胞分别置于３７℃．３９℃．４２℃下进行预处理，ＳＤＳ－ＰＡＧＦ、Ｎｏｒｔｈｅｍｂｌｏｔ及Ｗｅｓｔｅｍｂｌｏｔ显示４２℃预处理２ｈ导致心肌细胞中热休克蛋白（ＨＳＰｓ）特别是ＨＳＰ７０基因表达明显增加，并明显减轻了随后Ｈ２Ｏ２所致的心肌细胞损伤，表现为较高的细胞存活率、较高的ＳＯＤ及过氧化氢酶活性及较低的ＴＢＡＲＳ水平，而３９℃２ｈ的热休克预处理未能获得上述结果。在转录抑制剂放线菌素Ｄ或翻译抑制剂放线菌酮存在下，热休克预处理所诱导的ＨＳＰ基因表达被完全阻断，上述心肌细胞保护作用亦被完全取消。Primarily cultured chick embryo cardiomyocytes were pretreated with vari-, ous hyperthermal make - ups, i. e. heat shock pretreatment. lt was found that: (l ) Heat shock pretreatment (42℃. for 2 h) increased the gene expreseion of heat shock proteins (HSPs), especially HSP70, in the cardiomyocytes. (2) The same pretreatment (42 C for 2 h) decreased hydrogen peroxide - induced cell injury , as displayed by higher cell sur- vival rate, higher SOD and catalase activities and less TBARS accumulation in the cells. (3) The increased. HSPs gene expression and the protective effect induced by heat shock pretreatment can be completely abolished by the presence of actinotnycin D, an tran- scription inhibitor, or cyclohexiraide, an translation inhibitor. This work provided evi, dence for the myocardial pretective effect of HSPs on cell level. ,

关 键 词：热休克 过氧化氢 心肌 细胞损伤 

分 类 号：R542.2[医药卫生—心血管疾病]