肝脏缺血-再灌注后热休克蛋白70mRNA的表达

目的 :探讨缺血—再灌注后大鼠肝脏热休克蛋白 (HSP) 70mRNA的表达规律。方法 :通过已建立的大鼠肝脏缺血—再灌注模型 ,应用人HSP 70cDNA ,采用dotblot杂交 ,观察缺血—再灌注后大鼠肝脏HSP 70mRNA的表达。结果 :肝脏缺血 15min ,3 0min再灌注后没有HSP 70mRNA的表达 ,缺血 60min再灌注 2h伴有HSP 70mRNA的表达 ,高水平HSP 70mRNA的表达持续到再灌注 12h ,以再灌注 4h表达水平为最高。缺血 12 0min再灌注 2h ,HSP 70mRNA升高 ,高水平表达维持 4h ,再灌注 12hHSP 70mRNA消失。结论 :肝脏缺血—再灌注后可以诱导HSP 70mRNA的表达 ,必要的缺血时间所造成的肝脏损伤是HSP基因激活的基础 ,再灌注期间氧自由基的释放可能是其表达增加的原因。

Expression of Heat Shock Protein(HSP) 70mRNA in Ischemic-Reperfused Rat Liver

Objective: To explore the expression of heat shock protein 70mRNA in ischemic-reperfused rat liver. Methods: Changes in heat shock protein 70mRNA of rat liver were studied by dot blot hybridization using the ischemic-reperfused model of rat liver. Results: Short periods (15 or 30min) of liver ischemia was never followed by induction of HSP 70 genes after reestablishment of blood supply. Expression of HSP 70mRNA was found when 60min ischemia was followed by 2h blood reperfusion. High level HSP 70mRNA was maintained for the next 12h at least. Maximal induction of HSP 70mRNA occurred at 4h. The expression of HSP 70mRNA was increased at 2h of blood reperfusion after 120 minutes of ischemia. High level HSP 70mRNA expression was maintained for 4h. HSP 70mRNA disappeared completely 12h after restoration of the blood supply. Conclusion: The results indicate that blood reperfusion after temporary liver ischemia induces the expression of heat shock genes. The cell damage resulting from a certain duration of ischemia before reperfusion is essential for activation of heat shock genes. The possible reason of increases in HSP 70mRNA expression may be the release of oxygen free radicals during reperfusion.