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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 晶状体蛋白参与预适应的早期相保护机制提供了证据
The rat Langendorff perfused heart was used as a model to observe the changes of αB crystallin during the preconditioning phase. The results showed that the soluble αB crystallin in the cytoplasm migrated rapidly to the insoluble structure in the cells after ischemic preconditioning, gradually reset at 15min and 30min, and almost completely reset at 60min. After preconditioning, myocardial tolerance to ischemia-reperfusion injury was significantly enhanced, showing myocardial contractility and coronary flow was significantly higher than ischemia-reperfusion injury group, the release of creatine phosphokinase and myocardial malondialdehyde ( MDA content was significantly lower than ischemia-reperfusion injury group. These results suggest that ischemic preconditioning rapidly shifts the αB crystallin to intracellular insoluble structure and provides evidence for the involvement of αB crystallin in the preconditioning phase protection