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金雀异黄素对MCP-1诱导人脐静脉血管平滑肌细胞增殖及c-fos mRNA转录的影响 被引量:4

The inhibition of genistein on proliferation and transcription of c-fos mRNA in human umbilical vascular smooth muscle cells induced by MCP-1
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摘要 目的研究金雀异黄素对单核细胞趋化蛋白1(MCP1)诱导的人脐静脉血管平滑肌细胞(hUVSMC)增殖及cfosmRNA转录的影响。方法用不同浓度(10,30,90μmol·L-1)金雀异黄素预作用hUVSMC2h后加入终浓度为10μg·L-1的MCP1作用30min;采用逆转录聚合酶链反应检测细胞中cfos基因的表达;作用48h,用细胞计数检测细胞增殖的情况。结果金雀异黄素在低剂量(10μmol·L-1)即能抑制平滑肌细胞的增殖(P<0.05),在高剂量(30,90μmol·L-1)才能抑制细胞内cfosmRNA的表达(P<0.01,P<0.01)。结论金雀异黄素能抑制MCP1诱导的hUVSMC增殖,其机制可能与降低cfos的表达有关。 Aim To study the inhibition of genistein on proliferation and transcription of c-fos mRNA in human umbilical vascular smooth muscle cells ( hUVSMC ) induced by monocyte chemotactic protein-1 ( MCP-1 ). Methods Growth-arrested hUVSMC were stimulated with MCP-1 ( 10 μg· L^-1 ) prior to co-treatment with different concentrations of genistein ( 10,30,90 μmol· L^-1 ). The response of hUVMSC to these treatments was observed in comparison with that of control group. The proliferation of hUVMSC was evaluated by cell counting. The expression of c-fos mRNA was detected by RT-PCR. Results Low concentration of genistein (10 μmol· L^-1) inhibited the proliferation of hUVSMC and high concentration of genistein ( 30,90μmol·L^-1) inhibited the expression of c-fos in hUVSMC induced by MCP-1. Conclusions Genistein could suppress the proliferation of hUVSMC induced by of MCP-1. Its mechanisms may involve the down-regulation of c-fos mRNA expression.
出处 《中国药理学通报》 CAS CSCD 北大核心 2005年第8期943-946,共4页 Chinese Pharmacological Bulletin
基金 贵州省科技厅资金资助项目(No20033015)
关键词 金雀异黄素 MCP-1 C-FOS基因 动脉粥样硬化 genistein MCP-1 c-fos gene atherosclerosis
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参考文献14

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