Objective:The plasma expression levels of ET-1, TXB_2,6-keto-PGF_1α, vWF at different time after cerebral ischemia were assayed for observing the effects of baicalin, jasminoidin, cholalic acid, hydrolysis fluid of nacre and the combined prescription(CP) on cerebral vasoconstriction and endothelial cells in MCAO rats. Methods: The plasma levels of ET-1, TXB_2,6-keto-PGF_1α in MCAO rats were detected by the method of RIA and the plasma expressions of vWF were observed by ELISA. Results:The levels of ET-1, TXB_2/6-keto-PGF_1α and vWF all increased at different time after cerebral ischemia,so do TXB_2 at 12 hours after ischemia. The expression of 6-keto-PGF_1α significantly reduced at different time point after ischemia in MCAO rat. There were no significant changes after medicine treating 12 hours except baicalin's increasing 6-keto-PGF_1α level. Jasminoidin and CP significantly reduced the expression of ET-1 at 24 hours after ischemia, so do all effective components except CP on expression of TXB_2 at 12 hours after ischemia. The expression of TXB_2, was significantly decreased by baicalin and CP at 24 hours after cerebral ischemia. Both baicalin and cholalic acid significantly increased the expression of 6-keto-PGF_1α at 12 hours after ischemia while cholalic acid and hydrolysis fluid of nacre increased its level after ischemia for 24 hours.
TXB_2/6-keto-PGF_1α ratio was reduced distinctively by baicalin, jasminoidin, cholalic acid, CP at the point of 12 hours, while decreased by baicalin and CP, and increased by jasmionoidin at the point of 24 hours. On the other hand,baicalin, hydrolysis fluid of nacre significantly reduced and jasminoidin increased the expression of vWF at the point of 12 hours. At the point of 24 hours, expression of vWF reduced by hydrolysis fluid of nacre and increased by baicalin. Conclusions: The higher plasma expression of ET-1, TXA_2 in plasma aggravated cerebral vasoconstriction and damaged endothelial cells. At the same time, the effective components of "Qing Kai Ling" inhibit the expression of ET-1, TXA_2 and reduce both TXB_2/6-keto-PGF_1α ratio and level of vWF. As a result,they relax cerebral microvessel and protect endothelial cells by different pathway at different target points.