三乙酰莽草酸对血小板聚集的抑制作用  

INHIBITORY EFFECTS OF TRIACETYLSHIKIMIC ACID ON PLATELET AGGREGATION

作　　者：黄丰阳[1] 徐秋萍[1] 孙建宁[1] 郭亚健[1] 

机构地区：[1]北京中医药大学药理教研室

出　　处：《药学学报》1999年第5期345-348,共4页Acta Pharmaceutica Sinica

基　　金：国家科委"新药研究与产业化开发项目

摘　　要：目的：研究三乙酰莽草酸（ＴＳＡ）对血小板聚集功能的抑制作用及其作用机理。方法：用比浊法测定血小板聚集功能，分光光度法测定ＭＤＡ的含量，放免法测定ＴＸＢ２，６酮ＰＧＦ１α，ｃＡＭＰ和ｃＧＭＰ的含量。结果：ＴＳＡ１２５，２５，５０，１００和２００ｍｇ·ｋｇ－１ｉｇ明显抑制ＡＤＰ和胶原诱导的大鼠血小板聚集；ＴＳＡ１２５，５０和２００ｍｇ·ｋｇ－１ｉｇ显著增加大鼠血小板内ｃＡＭＰ水平，但不影响ｃＧＭＰ水平。ＴＳＡ２００ｍｇ·ｋｇ－１对ＡＡ诱导的血小板中ＭＤＡ的生成，ＡＤＰ诱导的血小板中ＴＸＢ２和腹主动脉壁６酮ＰＧＦ１α的生成有轻度抑制作用。结论：ＴＳＡ抑制血小板聚集作用部分与血小板内ｃＡＭＰ水平升高有关。AIM: To study the inhibitory effects of triacetylshikimic acid (TSA) on rat platelet aggregation and its mechanism. METHODS: Light transmission was used to measure platelet aggregation. Methods of spectrophotometry and radioimmunoassay were used to measure the levels of malondialdehyde(MDA), thromboxane B2(TXB2), 6ketoPGF1, cAMP and cGMP. RESULTS: TSA 125, 25,50,100 and 200 mgkg-1d-1 ig for 3 d inhibited the rat platelet aggregation induced by ADP and collagen. TSA 125, 50 and 200 mgkg-1 markedly increased the cAMP level and exhibited no effect on the cGMP level in rat platelets. TSA 200 mgkg-1 was shown to slightly inhibit AAinduced MDA generation and ADPinduced TXB2 formation in rat platelets, and to slightly suppress 6ketoPGF1 generation from the abdominal aortae. CONCLUSION: TSA was found to be a potent inhibitor of platelet aggregation, which was partially concerned with the elevation of cAMP in platelets.

关 键 词：三乙酰莽草酸 血小板聚集 6-酮-PGF1Α TXB2 

分 类 号：R973.2[医药卫生—药品]