金雀异黄酮的抗血小板聚集作用及机制

金雀异黄酮的抗血小板聚集作用及机制
范文蕾;罗丹
【期刊名称】《中国生化药物杂志》
【年(卷),期】2012(033)003
【摘要】目的观察金雀异黄酮对血小板聚集的影响,并初步探讨其作用机制.方法制备家兔富血小板血浆和贫血小板血浆,并通过加入不同浓度的金雀异黄酮,测定其对凝血酶和血小板活化因子( PAF)诱导的血小板聚集的抑制作用；并测定其对凝血酶的抑制率及PAF诱导聚集下的血栓素(TXB2)、6-酮-前列腺-F1α( 6-Keto-PGF1α)的水平.结果金雀异黄酮能明显抑制由凝血酶和PAF诱导的血小板聚集,且金雀异黄酮与凝血酶有一定的亲和力,在PAF诱导的血小板聚集中,金雀异黄酮能明显降低TXB2水平,升高6-Keto-PGF1α水平.结论金雀异黄酮能够明显抑制由凝血酶和PAF诱导的血小板聚集,其作用与抑制凝血酶有一定关系外,可能与其通过调节PAF诱导聚集TXA2和PGI2的释放有关.%Purpose To investigate the antiplatelet effect and mechanism of Cenistein. Methods The platelet poor plasma(PPP) and Platelet rich plasma(PRP) were used in our research. We evaluated rninhibitory activity in the assay of rabbit platelet aggregation induced by thrombin and platelet activating factors ( PAF) in vitro after adding drugs of different concentrations in PRP. The inhibition of drugs on thrombin and the plasma thromboxane B2(TXB2) ,6-Keto-PGF1α induced by PAF were evaluated as well. Results Genistein can effectively inhibit platelet aggregation, it has appropriate inhibition on thrombin, can reduce the TXB2 level and increase the 6-Keto-PGF1α level in the plasma induced
by PAF. Conclusion Genistein can effectively inhibit platelet aggregation induced by thrombin and PAF. The mechanism might be related to the suppression of thrombin and the regulation of PGI2 and TXA2 level after aggregation.
【总页数】3页(P267-269)
【作者】范文蕾;罗丹
【作者单位】武汉市妇女儿童医疗保健中心,湖北武汉430016;武汉市第三医院,湖北武汉430060
【正文语种】中文
【中图分类】R285
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