摘要
目的 :探讨没食子儿茶素没食子酸酯对巨噬细胞中由脂多糖 (LPS)激活的p38MAPK的作用特性及对肿瘤坏死因子 (TNF -α)表达的影响。方法 :在体外培养的小鼠巨噬细胞系中用Westernblotting检测p38MAPK磷酸化水平 ,应用酶联免疫吸附法检测巨噬细胞表达TNF -α的水平 ,利用电镜观察EGCG对LPS结构的影响。结果 :LPS刺激巨噬细胞引起p38MAPK磷酸化程度和TNF -α表达明显增高 ,EGCG对LPS激活的p38MAPK磷酸化和TNFα的表达有明显的抑制作用 ,EGCG对LPS的结构无显著影响。结论 :EGCG对LPS无直接的拮抗作用 ,而是通过干预体内信号通路发挥其抑制作用 ,p38MAPK可能是EGCG抑制LPS诱导巨噬细胞表达TNF
AIM: To investigate the effect of epigallocatechin-3-gallate (EGCG) on lipopolysaccharide (LPS)-induced p38 MAPK activation and tumor necrosis factor-α (TNF-α) secretion in macrophages. METHODS: Western blotting was used to detect the phosphorylation of p38 MAPK in mouse macrophages cultured in vitro. Enzyme linked immunosorbent assay was used to determine the secretion of TNF-α in macrophages. Electron microscopy was used to study the effect of EGCG on the structure of LPS. RESULTS: LPS caused activation of p38 MAPK and more production of TNF-α, EGCG inhibited LPS-induced phosphorylation of p38 MAPK and TNF-α production and had no effect on the structure of LPS. CONCLUSIONS: EGCG has no direct effect on LPS, but blocks cellular signal pathway. The inhibition of EGCG on LPS-induced TNF-α production is mediated, at least in part, through blocking of p38 MAPK pathway. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第10期1814-1818,共5页
Chinese Journal of Pathophysiology
