内毒素对大鼠原代肝星状细胞ERK1/2信号转导通路的影响  

Effect of endotoxin on ERK1/2 pathway of rat primary HSCs in vitro

作　　者：张银枝[1] 徐军全[2] 陈峰杰[1] 康杰[2] 姚瑞强[2] 王明亮[2] 

机构地区：[1]山西医科大学,太原030001 [2]山西医科大学汾阳学院,032200

出　　处：《中国医疗前沿》2012年第3期35-37,共3页China Healthcare Innovation

基　　金：山西省回国留学人员科研资助项目(编号:2002-74)

摘　　要：目的研究内毒素对大鼠原代肝星状细胞(hepatic stellate cells,HSCs)增殖活化过程中ERK1/2信号转导通路的影响及机制。方法用链霉蛋白酶、Ⅳ型胶原酶以及密度梯度离心法分离培养大鼠原代HSCs,随机分为对照组、内毒素组和PDTC(Pyrrolidinedithiocarbamic acid,NF-κB抑制剂)组。在培养至第5d时,内毒素组和PDTC组加入终浓度为lμg/ml的内毒素刺激细胞,PDTC组同时加入终浓度为15μmol/L的PDTC,30min后收集各孔HSCs,提取细胞总蛋白,Western Blot检测P-ERK1/2水平。结果内毒素刺激原代培养HSCs后,与对照组相比P-ERK1/2水平明显上升(P<0.01),NF-κB抑制剂PDTC能显著降低该变化。结论内毒素可直接刺激大鼠原代HSCs引起胞内ERK1/2信号传导通路活化,NF-κB信号通路可能是内毒素刺激的原代HSCs所导致ERK1/2信号转导通路活化的重要途径之一。Objective To investigate the influence of endotoxin on ERK1/2 pathway of rat primary HSCs in vitro.Methods HSCs were isolated from rats liver by the method of enzymatic digestion and density gradient centrifugation,and randomized into endotoxin group,PDTC（Pyrrolidinedithiocarbamic acid,inhibitor of NF-κB） group and control group.After 5 days normal cultivation,endotoxin and PDTC groups add endotoxin（lμg/ml）,PDTC group add PDTC（15μmol/L） as well,the levels of P-ERK1/2 were measured by western blot after incubation for 30 minutes.Results The level of P-ERK1/2 increased significantly after HSCs were stimulated directly by endotoxin,compared with the control group（P 0.01）,incubated with PDTC can partly prevent this change（P 0.05）.Conclusions Endotoxin can directly stimulate ERK signaling pathway of HSCs,and NF-κB signaling pathway may play an important role in this process.

关 键 词：内毒素 肝星状细胞 NF-ΚB ERK 肝纤维化 

分 类 号：R575.2[医药卫生—消化系统]