摘要
目的观察染料木黄酮(genistein,Gen)对3T3-L1脂肪细胞炎症因子表达和分泌的影响并探讨其作用机制。方法体外培养3T3-L1前体脂肪细胞,诱导细胞分化,以脂多糖(lipopolysaccharide,LPS)建立炎症模型,采用QRT-PCR和ELISA检测Gen对LPS诱导的脂肪细胞炎症因子肿瘤坏死因子α(TNF-α)、白介素6(IL-6)、单核细胞趋化蛋白-1(MCP-1)表达和释放的影响;Western blot检测Gen对脂肪细胞中p65表达及p65(ser536)磷酸化水平影响。结果 Gen抑制LPS诱导脂肪细胞产生并释放TNF-α、IL-6和MCP-1,且抑制作用呈剂量-效应关系;Gen抑制LPS所诱导的p65磷酸化水平的增加。结论 Gen抑制LPS对脂肪细胞炎症反应的诱导,而这一作用机制之一是通过抑制脂肪细胞NF-κB通路的激活。
【Objective】 To investigate the effect of genistein（Gen） on LPS-induced inflammatory response in 3T3-L1 adipocytes and to discuss its functional mechanism.【Methods】 3T3-L1 preadipocytes were cultured in vitro and were differentiated into the matured adipocytes.The effects of Gen on the expression and secretion of TNF-α,IL-6 and MCP-1 in 3T3-L1 adipocytes induced by LPS were determined by QRT-PCR and ELISA.The effect of Gen 1on p65（ser536） phosphorylation level was detected by Western blot.【Results】 Gen inhibited the expression and secrection of TNF-α,IL-6 and MCP-1 in 3T3-L1 adipocytes cells induced by LPS,and the inhibitory effects appeared in a dose-dependence manner.Gen down-regulated the level of p65（ser536） phosphorylation induced by LPS.【Conclusion】 Gen suppresses the LPS-induced inflammatory response in 3T3-L1 adipocytes and its effect is involved in the inhibitory effects of Gen on NF-κB pathway activation.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2013年第13期29-32,共4页
China Journal of Modern Medicine
