甲基乙二醛对Jurkat细胞氧化应激及分泌细胞因子的影响  

Effects of methylglyoxal on oxidative stress and cytokine profiles in cultured Jurkat cells

作　　者：游捷[1] 余洪根[1] 彭雪峰[1] 刘晓红[1] 刘礼斌[1] 

机构地区：[1]福建医科大学附属协和医院内分泌科福建省内分泌研究所,福州350001

出　　处：《中国免疫学杂志》2011年第7期583-587,共5页Chinese Journal of Immunology

基　　金：福建省自然科学基金计划资助项目(C0710017)

摘　　要：目的：探讨甲基乙二醛（MGO）对Jurkat细胞氧化应激及分泌细胞因子的影响。方法：不同浓度MGO作用PHA预刺激的Jurkat细胞,MTT检测细胞生长,流式细胞检测细胞内活性氧（ROS）,Western blot检测p38 MAPK、JNK磷酸化水平,ELISA检测TNF-α、IFN-γ。结果：1560μmol/L MGO对Jurkat细胞生长无影响,但能使ROS呈浓度依赖性升高;N-乙酰-L-半胱氨酸（NAC）和氨基胍（AG）能明显抑制此作用。MGO作用30分钟,pp38/p38、pJNK/JNK明显升高。MGO诱导Jurkat细胞分泌TNF-α、IFN-γ;P38、JNK抑制剂及NAC能降低TNF-α、IFN-γ的分泌。结论：MGO能诱导Jurkat分泌TNF-α、IFN-γ;其机制可能通过氧化应激、P38、JNK信号通路。Objective：To investigate the effects of methylglyoxal（MGO） on oxidative stress and cytokine profiles in cultured Jurkat cells for understanding more about the mechanism of diabetes accelerated athevosclerosis.Methods：Jurkat cells which pre-stimulated by PHA were incubated with MGO for 24 h.The cells survival rate was detected by MTT.ROS was quantitated by flow cytometry.Total and phosphorylated p38 and JNK were assessed using Western blot.After incubation with MGO,the expression of TNF-α and IFN-γ were tested by ELISA.Results：No changes in cells viability was observed when Jurkat cells were treated with 0-60 μmol/l MGO.Incubation of Jurkat cells with MGO significantly induced ROS production.Co-incubation with NAC or AG decreased MGO-induced ROS production.Incubation of Jurkat cells with MGO results in significant increase in p38 and JNK phosphorylation.In addition MGO significantly increased the production of TNFα and IFN-γ while p38,JNK inhibitor and NAC reversed the secretion of pro-inflammatory cytokines.Conclusion：These data demonstrate that MGO induced the release of TNF-α and IFN-γ in Jurkat cells via oxidative stress,p38,JNK signaling pathway.

关 键 词：甲基乙二醛 JURKAT细胞 氧化应激 细胞因子 动脉硬化 

分 类 号：R392.6[医药卫生—免疫学]