《中国康复理论与实践》

《中国康复理论与实践》 ›› 2006, Vol. 12 ›› Issue (04): 301-303.

• 基础研究 • 上一篇    下一篇

HSP27在大鼠心肌细胞缺氧预处理中的保护作用及其机制

张雪松; 张雪岩; 杨秀娟; 郭宏; 辛险峰; 曾繁荣; 左会明   

  1. 佳木斯大学附属第一医院麻醉科 黑龙江佳木斯市 154002
  • 收稿日期:2005-11-21 出版日期:2006-04-25 发布日期:2006-04-25

Protective Effect of Heat Shock Protein 27 on Cardiomyocytes when Ischemic Preconditioning Performed in Rat

ZHANG Xue-song,ZHANG Xue-yan, YANG Xiu-juan, et al   

  1. The Department of Anesthesiology, First Clinical Hospital Affiliated Jiamusi University, Jiamusi 154002, Heilongjiang, China
  • Received:2005-11-21 Published:2006-04-25 Online:2006-04-25

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摘要： 目的探讨大鼠心肌细胞缺氧预处理中热休克蛋白27(HSP27)的保护作用及其机制。方法将原代培养的心肌细胞分为4组正常对照组、缺氧组、缺氧预处理组和放线菌酮抑制组。MTT法观察处理后各组细胞的活力;DNA ladder、Annexin Ⅴ-FITC流式细胞仪检测心肌细胞凋亡;免疫印迹法检测各组中HSP27、casPase-3的表达。结果缺氧预处理可诱导HSP27产生,明显增加细胞活力,细胞凋亡率明显降低,且降低casPase-3的表达;翻译抑制剂放线菌酮完全阻断了缺氧预处理诱导的HSP27的基因表达,上述细胞保护作用亦被完全取消。结论缺氧预处理诱导的HSP27对心肌细胞起保护作用,机制可能与HSP27对抗细胞凋亡有关。

关键词: 热休克蛋白27, 缺氧预处理, 心肌细胞, 凋亡, caspase-3

Abstract: ObjectiveTo investigate the mechanism and the protective effect of heat shock protein 27 (HSP27) on rat cardiomyocytes when ischemic preconditioning performed.MethodsCultured rat cardiomyocytes were divided into four groups: control group, ischemic group,ischemic preconditioning group and cyclohexamide group. Cell viabilities were analyzed by MTT. The apoptosis was evaluated with DNA ladder and flow cytometry Annexin V Flous staining. Western Blot was used to determine the expression of HSP27 and caspase-3 in cardiomyocytes.ResultsIschemic preconditioning could improve cell viability. The apoptosis ratio in ischemic preconditioning group was significantly less than that in ischemic group. These were accompanied by an increase in the expression of HSP27 and a decrease in caspase-3. The expression of the increased HSP27 and the protective effect induced by ischemic preconditioning were completely abolished by the presence of cycloheximide, a translation inhibitor.ConclusionThe expression of HSP27 induced by ischemic preconditioning plays an important role in protecting cardiomyocytes, and the mechanism is possibly related to the inhibition of cell apoptosis.

Key words: heat shock protein 27 (HSP27), ischemic preconditioning, cardiomyocyte, apoptosis, caspase-3