为探讨雌激素和异黄酮类药物对内皮细胞粘附分子 CD5 4表达的影响 ,作者采用 10 ng/ ml肿瘤坏死因子 (TNFα)处理人脐静脉内皮细胞 6小时 ,并加用不同浓度的异黄酮 (WZ1 ,WZ2 )和雌激素 (WZ3,WZ4)进行干预 48小时 ,而后用流式细胞仪定量测定细胞表面粘附分子 CD5 4的表达 ,并进行统计学分析。结果 :110 ng/ ml的TNFα可使内皮细胞表面粘附分子 CD5 4的表达升高 4倍 ,与对照组相比具有统计学差异 (P<0 .0 5 ) ;2 10 - 1 0 m ol/L、10 - 8m ol/ L、10 - 6 m ol/ L 异黄酮和异卟黄酮对由 TNFα诱导的内皮细胞的 CD5 4表达有轻度促进作用 ;3哌嗪雌酚酮和雌二醇预处理内皮细胞 48小时后再加 TNFα激活 ,内皮细胞表面 CD5 4平均荧光强度与单纯 TNFα组相比下降明显 (P<0 .0 5 ) ,各浓度组之间不具统计学差异 (P>0 .0 5 )。以上结果提示 :异黄酮和异卟黄酮对内皮细胞粘附分子 CD5 4的表达无抑制作用 ;哌嗪雌酚酮和雌二醇可在一定程度上抑制 CD5 4的表达 ,从而为抗粘附疗法提供了一条新思路。 To investigate the effect of estrogen and isoflavones on the expression of endothelial cell adhesion molecule CD5 4, we treated human umbilical vein endothelial cells with 10 ng / ml tumor necrosis factor (TNFα) for 6 hours and treated with different concentrations of isoflavones (WZ1, WZ2) and estrogen (WZ3, WZ4) for 48 hours. Then the expression of cell surface adhesion molecule CD5 4 was quantified by flow cytometry and analyzed statistically. Results: TNFα at a concentration of 110 ng / ml increased the expression of CD54 on the surface of endothelial cells, which was significantly higher than that of the control group (P <0.05) / L, 10 -8 mol / L and 10 -6 mol / L isoflavone and isoprotectin could promote the CD54 expression of endothelial cells induced by TNFα slightly. 3 Praziquantel and estradiol 48 hours after pretreatment of endothelial cells plus TNFα activation, the average fluorescence intensity of CD5 4 on endothelial cells decreased significantly compared with that of TNFα alone group (P <0.05), and there was no significant difference between each concentration group (P> 0) .0 5). The above results suggest that isoflavone and isoporphyrin flavonoids have no inhibitory effect on the expression of endothelial cell adhesion molecule CD5 4; piperazinyl estrone and estradiol can inhibit the expression of CD5 4 to a certain extent, Provide a new idea.