αB-晶状体蛋白在大鼠心肌缺血预适应早期相中的作用

The roles of αB-crystallin during early phase of myocardial ischemic preconditioning in rats

以大鼠Langendorff离体灌流心脏为模型 ,观察αB 晶状体蛋白在预适应早期相保护阶段的变化。结果显示 :经缺血预处理后胞浆中可溶性αB 晶状体蛋白迅速移位至细胞内的不溶性结构中 ,15min ,30min逐渐复位 ,6 0min时已接近全部复位。经预适应后的心肌对缺血再灌流损伤的耐受性明显增强 ,表现为心肌收缩力及冠脉流量明显高于缺血 再灌损伤组 ,肌酸磷酸激酶释放率及心肌丙二醛 (MDA)含量明显低于缺血 再灌损伤组。提示缺血预适应使αB 晶状体蛋白迅速移位于细胞内不溶性结构 ,为αB

Objective: This study designed to observe intracellular translocation of αBcrystallin, a small heat shock protein, and its possible implication during the early phase of myocardial ischemic preconditioning in isolated Langendorff rat hearts. Eighteen male Wistar rats(180～250?g) were randomly divided into three groups: ① Control group(Ctrl) was perfused with KH solution throughout the experiment; ② ischemiareperfusion group(IR) experienced 30?min of global ischemia and 120?min of reperfusion and ③ preconditioning and ischemiareperfusion group(PC+IR) was preconditioned with three cycles of short myocardial ischemia(5?min each, seperated by 5?min of reperfusion) prior to 30?min of ischemia and 120?min of reperfusion. It was showed that cytosolic soluble αBcrystallin rapidly translocated to insoluble intracellular structure after ischemic preconditioning, then gradually returned to soluble cytosol pool and almost completely recovered at about 60?min after preconditioning. In the meanwhile, ischemic preconditioning markedly alleviated subsequent myocardial ischemiareperfusion injury, as indicated by the improvement of LVP,+dp/dt max, coronary flow, heart rate, CPK release and malondialdehyde(MDA) production. The results suggest that the intracellular translocation of αBcrystallin might be important for myocardial protection during the early phase of ischemic preconditioning. [