双歧杆菌脂磷壁酸通过激活小鼠腹腔巨噬细胞MEK/ERK通路促进TNF-α的表达

Lipoteichoic acid from bifidobacterium up-regulated the expression of TNFα by activating MEK/ERK signaling pathway in mice peritoneal macrophage

目的:本研究分析激活的MEK/ERK信号通路在双歧杆菌脂磷壁酸促进小鼠腹腔巨噬细胞肿瘤坏死因子-α(TNF-α)增强表达中参与的机制。方法 :分离小鼠腹腔巨噬细胞并随机分为3组:对照组、脂磷壁酸组和脂磷壁酸+PD98059组(n=6)。酶联免疫吸附测定法检测各组巨噬细胞中TNF-α的含量,Western Blotting检测各组巨噬细胞中MEK/ERK信号通路的关键蛋白Ras、Raf、pMEK/MEK、pERK1/2及ERK1/2的表达。结果:与对照组相比,脂磷壁酸组小鼠巨噬细胞的TNF-α水平明显增高,差异具有统计学意义(P<0.01);MEK/ERK信号通路相关蛋白Ras、Raf、pMEK/MEK、pERK1/2及ERK1/2的表达明显上调,差异具有统计学意义(P<0.01),而PD98059可以明显抑制上述蛋白的异常(P<0.01)。结论:双歧杆菌脂磷壁酸通过激活小鼠腹腔巨噬细胞MEK/ERK通路促进TNF-α的上调表达。

Objective：To investigate the mechanism of TNFαup-regulation in mice peritoneal macrophage induced by lipoteichoic acid from Bifidobacterium.Methods：Mice peritoneal macrophage were divided in to 3groups：control,lipoteichoic acid and PD98059 group.The content of TNFαin each group was detected by ELISA and the expression of MEK/ERK signaling pathway proteins were assayed by Western Blotting.Results：The result showed that the content of TNFαwas increased greatly（P〈0.01）in lipoteichoic acid group while PD98059 can decrease it greatly（P〈0.01）.The result also showed that the MEK/ERK pathway proteins Ras,Raf,pMEK/MEK,pERK1/2as well as ERK1/2 were up-regulated dramatically（P〈0.01）.PD98059 also signified effectiveness in inhibiting it（P〈0.01）.Conclusion：Lipoteichoic acid from Bifidobacterium enhances the expression of TNF-αby activating MEK/ERK signaling pathway in mice peritoneal macrophage.