大鼠脑缺血再灌后凝血酶与PAR-1的表达及意义

目的探讨大鼠脑缺血再灌后凝血酶（thrombin）及蛋白酶活化受体-1（PAR-1）的表达变化及意义。方法栓线法制作大鼠大脑中动脉闭塞再灌注模型，用Western Blot方法检测对照组及脑缺血2h再灌注不同时程组（12、24h，3、7d）凝血酶和PAR1蛋白表达水平。结果对照组可以检测到少量凝血酶（thrombin）和PAR-1的表达，两种蛋白于再灌注12h显著上升。3d达高峰（P〈0．01），7d下降；缺血再灌注后凝血酶与PAR-1的表达呈高度正相关（r=0．934，P〈0．01）。结论凝血酶和PAR-1蛋白的表达增加可能与脑缺血冉灌注损伤的发病机制有关；凝血酶可能通过激活PAR-1参与了再灌注损伤的病理生理过程。

The expression and significance of thrombin and PAR-1 following focal cerebral ischemia reperfusion in rats

Objective To investigate the expression of thrombin and protease-activated receptor-1 in the brain tissue of rats after cerebral ischemia reperfusion. Methods The focal cerebral isehemia and reperfusion model was induced by ligation with nylon monofflament in rats. Thrombin and PAR-1 protein levels in the control group and the cerebral ischcmic reperfusion groups at 12 h,24 h,3 d and 7 d were detected by Western Blot method. Results Western Blot experiments indicated that a low level of thrombin and PAR l were detected in the control group. The expression level of those two protein increased significantly at 12 h after reperfusion, peaked at 3 d（P〈0.01 ） ,then began to decline at 7 d in the ischemia cortex of ischemic reperfusion groups. The expression of zbrombin was highly positive correlation with the PAR1 （r = 0.934,P〈0.01 ） after ischemic reperfusion. Conclusions It is likely that the increased expression of thrombin and PAR1 are associated with the pathogenesis of ischemia reperfusion induced injury. Thrombin exerts its effects in the pathophysiology of cerebral ischemia reperfusion injury through activating PAR-1.