黄芩苷对脂多糖诱导的巨噬细胞NF-κB活化和炎症因子表达的影响

Effect of Baicalin on Activity of NF-κB and Expression of Inflammatory Cytokines in LPS-stimulated Macrophage Cells

目的:研究黄芩苷对脂多糖(LPS)诱导小鼠巨噬细胞核因子κB(NF-κB)及肿瘤坏死因子α(TNF-α)、白介素6(IL-6)表达的影响。方法:分别用LPS(终浓度1μgomL-1)和LPS+黄芩苷(终浓度10,50,100μmolmoloL-1)处理生长良好的小鼠巨噬细胞RAW264.7,用RT-PCR法和Elisa法检测细胞及其上清液中TNF-α、IL-6mRNA和蛋白的表达变化,用Western Blot法检测细胞核内NF-κBp65蛋白含量变化。结果:LPS刺激RAW264.7细胞可导致NF-κB激活,上调TNF-α、IL-6表达;黄芩苷预处理能降低LPS诱导的NF-κB活化和TNF-α、IL-6表达。结论:黄芩苷可通过抑制NF-κB活化,下调LPS诱导的巨噬细胞TNF-α、IL-6的生成,发挥抗炎作用,这可能是其抗动脉粥样硬化的作用机制之一。

Objective：To investigate the inhibitory effects of baicalin on the activation of nuclear factor kappa B （NF-κB） and investigate the expression of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in macrophage cell lines RAW264.7 induced by lipopolysaccharide （LPS）. Methods： RAW264.7 cells were cultured in vitro, and treated with different concentration of baicalin in the presence or absence of LPS for different time. The mRNA and protein expression of TNF-αand IL-6 were determined by RT-PCR and Elisa, respectively. The expression of NF-κB p65 in the nuclei was determined by Western Blot. Results： The expression of TNF-α and IL-6 were markedly up-regulated and the expression of NF-κB p65 also significantly increased in macrophage cells stimulated with LPS. Pretreated with baicalin inhibited LPS-induced TNF-α and IL-6 expression in both mRNA and protein levels, as well reduced the activation of NF-κβ. Conclusions： Baicalin effectively down regulated TNF-α and IL-6 expression in LPS-induced macrophage cells by inhibited the activation of NF-κβ. which may be one of its antiatherosis actions.