3，4＇，5－三羟基芪－3－β－单－D－葡萄糖甙在血小板血管内皮混合细胞中调节TXA2／PGI2生成的作用  

The regulation effect of 3, 4', 5-trihydroxystibene --3-β-mono--D--glucoside (Pol)on TXA2/PGI2 in the mixed preparation of platelet and vascular endothelial cells

作　　者：张佩文[1] 王耀忠[1] 余传林[1] 骆苏芳[1] 

机构地区：[1]第一军医大学药理学教研室

出　　处：《中药药理与临床》1994年第3期23-25,共3页Pharmacology and Clinics of Chinese Materia Medica

摘　　要：在血小板－脐静脉内皮细胞混合制备中，Ｐｏｌ０．０７０～１．１５４ｍｍｏｌ／Ｌ呈剂量依赖性显著降低凝血酶升高ＴＸＡ２的作用．Ｐｅｌ１．１５４ｍｍｏｌ／Ｌ也显著降低ＡＡ升高ＴＸＡ２的作用，但均不降低凝血酶或ＡＡ升高ＰＧＩ２的作用，结果使ＴＸＡ２／ＰＧＩ２比值下降；Ａｓｐｉｒｉｎ０．７２ｍｍｏｌ／Ｌ不只抑制凝血酶和ＡＡ升高ＴＡＸ２的作用，也抑制其升高ＰＧＩ２的作用，只是对前者的抑制强于后者，使ＴＸＡ２与ＰＧＩ２比值亦趋于下降。当细胞处于基础状态时，以上Ｐｏｌ与Ａｓｐ对ＴＸＡ２、ＰＧＩ２的生成均无影响。ol 0. 070 - 1. 154 mmol. L-1 dose--dependently reduced the increase effect of TXA2 induced bythrombin in the mised prepertion of platelet and umbilical vein endothelial cells. Pol 1. 154 mmol. L-1 alsosignificantly reduced the increase effect of TXA2 induced by arachidonic acid (AA). However, Pol did notreduce the increase effed of PGI2 induce by thrombin or AA and the ratio of TXA2 and PGI2 was declining. Aspirin 0. 72 mmol. L-1 not only depressed the increase effect of TXA2 but also inhibited the increaseeffect of .PGI2 induced by thrombin or AA. The inhibitory effect of aspirin on TXA2 was stronger than thaton PGI2 and TXA2/PGI2 showed declining. Either Pol or aspirin had no influence on the production of TXA2or PGI2 when the mind preparation was not treated with thrombin or AA.

关 键 词：PGI2 TXA2 升高 凝血酶 血小板 混合细胞 血管内皮 D-葡萄糖 羟基 降低 

分 类 号：R743[医药卫生—神经病学与精神病学] R719.8[医药卫生—临床医学]