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目的:旨在观察小窝蛋白-1(caveolin-1)在17β-雌二醇(E2)抑制脂多糖(LPS)诱导的大鼠胸主动脉血管平滑肌细胞(VSMCs)分泌单核细胞趋化蛋白-1(MCP-1)中的作用。方法:原代培养VSMCs,以不同浓度E2(10-9-10-6mol/L)干预LPS诱导的MCP-1的分泌,ELISA法检测MCP-1生成的变化。分别使用caveo-lin-1的阻断剂β-甲基环糊精(β-MCD)以及特异性caveolin-1 siRNA抑制caveolin-1表达,W estern b lotting法检测caveolin-1蛋白表达的变化。结果:LPS浓度和时间依赖地诱导MCP-1的表达,不同浓度E2(10-9-10-6mol/L)抑制LPS诱导的MCP-1的表达;分别使用β-MCD以及caveolin-1 siRNA抑制caveolin-1的表达,能抑制LPS诱导的MCP-1的表达,而E2(10-6-10-9mol/L)又可以抑制caveolin-1的表达。结论:E2抑制LPS诱导的血管平滑肌细胞MCP-1的表达,caveolin-1是这一抑制作用的中间环节。
OBJECTIVE: To investigate the effect of caveolin-1 on the secretion of monocyte chemoattractant protein from rat aortic vascular smooth muscle cells (VSMCs) induced by lipopolysaccharide (LPS) by 17β-estradiol (E2) -1 (MCP-1). Methods: Primary cultured VSMCs were treated with different concentrations of E2 (10-9-10-6mol / L) to interfere with the secretion of MCP-1 induced by LPS and the changes of MCP-1 production by ELISA. The caveolin-1 expression was inhibited by the caveolin-1 inhibitorβ-methylcyclodextrin (β-MCD) and caveolin-1 siRNA respectively. The expression of caveolin-1 protein was detected by Western blotting. Results: The expression of MCP-1 was induced by LPS in a concentration-dependent and time-dependent manner. Different concentrations of E2 (10-9-10-6 mol / L) inhibited the LPS-induced MCP-1 expression and the inhibitory effect of β-MCD and caveolin- The expression of caveolin-1 can inhibit the LPS-induced MCP-1 expression, while E2 (10-6-10-9 mol / L) can inhibit the expression of caveolin-1. Conclusion: E2 inhibits the expression of MCP-1 induced by LPS in vascular smooth muscle cells. Caveolin-1 is the intermediate part of this inhibition.