EGCG通过ERK1／2途径抑制LPS诱导人单核细胞产生前炎性细胞因子

目的探讨表没食子儿茶素没食子酸酯（EGCG）在体外对脂多糖诱导人单核细胞产生前炎症细胞因子TNF-α、IL-6和IL-1β的影响以及可能的调控机制。方法体外培养人单核细胞THP-1，将5～30μmolEGCG与之共同孵育后加入脂多糖刺激，酶联免疫吸附试验（ELISA）检测TNF-α、IL-6和IL-1β的产生情况。提取刺激后的细胞总蛋白，Western blot检测ERK1／2的磷酸化情况。结果当THP-1细胞首先与EGCG处理后，能显著降低LPS诱导的TNF-α、IL-1β和IL-6产生，同时EGCG能抑制ERK1／2的磷酸化。细胞经ERK1／2特异性抑制剂U0126处理后，EGCG能进-步降低细胞因子的产生。结论EGCG能抑制LPS诱导人单核细胞产生前炎症细胞因子，可能是通过抑制ERK1／2的磷酸化而实现的。

EGCG Inhibits LPS-induced Cytokines Production Through ERK1/2 Pathways in Human Monocyte Cells

Objective To study the effect and possible regulatory mechanism of Epigallocatechin gallate （EGCG） on lipopolysaccharide induced monocyte cells production of pro-inflammatory cytokines in vitro. Methods Cultured THP-1 cells were preincubated with 5 -30 μmol EGCG before LPS stimulation,then the ELISA was used to detect the production of TNF-α ,IL-6 and IL-1β. After then extracting the total cellular protein,phosphorylation of ERK1/2 was detected by western blot. Results When THP-1 cells first treated with EGCG,they could significantly reduce LPS-induced TNF-α ,IL-1β and IL-6 production,simultaneously EGCG inhibited ERK1/2 phosphorylation. Cells which were treated by ERK1/2 Specifical inhibitor UO126,EGCG could further reduce the production of cytokines. Conclusion EGCG could inhibited LPS induce monocyte to produce proinflammatory cytokines,and possibly achieved by inhibiting ERK1/2 phosphorylation.