摘要
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.
出处
《现代生物医学进展》
CAS
2009年第22期4219-4221,4278,共4页
Progress in Modern Biomedicine
基金
国家自然科学基金(30901980)
广东省高校重点培养青年教师基金(K5090005)
关键词
黄芩苷
巨噬细胞
细胞因子
核因子κκB
内毒素
Baicalin
Macrophage cell
Cytokine
Nuclear factor kappa B
Lipopolysaccharide