摘要
目的:研究黄芪中毛蕊异黄酮对雌激素受体(ER)活性的影响,考察它对人脐静脉内皮细胞(HUVEC)的促增殖作用并对其机制进行初步探讨。方法:用GeneBLAzerβ-内酰胺报告基因模型检测毛蕊异黄酮与ERα和ERβ的关系;XTT法检测毛蕊异黄酮对细胞增殖的影响;免疫印记杂交观察给药后磷酸化ERK1/2的表达。结果:毛蕊异黄酮能产生较弱的ERα和ERβ激动剂效应,可明显拮抗雌二醇对ERα和ERβ的活性;XTT实验表明毛蕊异黄酮能促进HUVEC增殖,在100μM效果最明显,增殖率达41%;ER抑制剂ICI182,780明显抑制毛蕊异黄酮介导的HUVEC增殖,增殖率下降约40%;免疫印记杂交的结果显示毛蕊异黄酮能快速激活ERK1/2磷酸化。结论:毛蕊异黄酮作为一种ER部分激动剂能通过ER促进HUVEC增殖,其促增殖活性与ERK1/2的激活有关。
Purpose：This study was designed to examine whether calycosin,a major isoflavonoid in Radix Astragali,acts on estrogen receptor and promotes human endothelial cells proliferation.Methods：Calycosin was found to induce HUVEC proliferation as measured by XTT assay.The involvement of activation of ERK1/2 in the proliferation stimulating effect was examined by Western blot.GeneBLAzer β-lactamase reporter assay was used to determine the agonistic/antagonistic activity of calycosin against both ERα and ERβ.Since calycosin selectively modulated ER transcriptional activation activities,the effect of ER inhibitor on calycosin-induced HUVEC proliferation was examined.Result：The agonism of ERα and ERβ induced by calycosin was slight,while the antagonism was significant.Calycosin promoted the HUVEC proliferation in a dose-dependent manner,and calycosin simulated rapid phosphorylation of ERK1/2 and reached maximum at 30~60min.and this effect can be reversed by ER inhibitor ICI182,780.In addition,the proliferation effect could be abolished by ER inhibitor ICI182,780.Conclusion：Calycosin,acts as a partial agonist of ER,promotes HUVEC proliferation involving activation of estrogen receptor and ERK1/2 signaling pathway.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2009年第6期14-17,共4页
Pharmacology and Clinics of Chinese Materia Medica
基金
澳门科技发展基金资助项目(045/2007/A3)
澳门大学研究委员会资助项目(RG085/07-08S/09R)
