表没食子儿茶素-3-没食子酸酯抑制脂多糖诱导的巨噬细胞促炎因子TNF-α和IL-1β基因表达

表没食子儿茶素-3-没食子酸酯(epigallocatechin-3-gallate,EGCG)具有抗氧化、抗癌、抗炎等多种生物学特性,但对巨噬细胞中表达TNF-α及IL-1β的报告尚存在争议.本文旨在探索EGCG对脂多糖(LPS)诱导的小鼠腹腔巨噬细胞和RAW264.7细胞促炎细胞因子Tnf-α和Il-1β基因表达的影响.MTT结果显示,0~100μmol/L EGCG对RAW264.7细胞活力没有影响;实时荧光定量PCR(qRT-PCR)和ELISA分析显示,1 mg/L LPS可显著升高小鼠腹腔巨噬细胞和RAW264.7细胞Tnf-α和Il-1βmRNA和蛋白水平,EGCG单独处理对巨噬细胞Tnf-α和Il-1β的基因表达与蛋白生成没有影响,但可以抑制LPS诱导的巨噬细胞Tnf-α和Il-1β的基因表达与蛋白生成,并存在剂量依赖效应.上述结果提示,EGCG可以剂量依赖方式抑制LPS诱导的巨噬细胞促炎细胞因子Tnf-α和Il-1β的表达,这可能与EGCG的抗炎效应有关.

Epigallocatechin-3-gallate Inhibits LPS-induced Gene Expression of TNF- αand IL-1β in Murine Macrophage

Epigallocatechin-3-gallate (EGCG) has various pharmacological activities, including anticancer, anti-oxidative and anti-inflammatory effects. However, whether EGCG affects the expression of proinflammatory cytokines of Tnf-α and Il-1β in macrophage is still in dispute. This study aimed to characterize the effect of EGCG on lipopolysaccharide (LPS)-induced Tnf-α and Il-1β expression in murine peritoneal and RAW264-7 macrophages. The MTT results showed that EGCG did not exert cytotoxicity at tested concentrations of 0 ～ 100 μmol/L in RAW264-7 cells. The qRT-PCR and ELISA results showed that 1 mg/L LPS stimulated the mRNA and protein levels of Tnf-α and Il-1β, but not EGCG treatment alone. In fact, EGCG inhibited LPS-induced Tnf-α and Il-1β expression and protein secretion in a dose-dependent manner. Our results suggested that EGCG inhibited LPS-induced pro-inflammatory gene expression for its anti-inflammatory effects.