LPS诱导L929细胞β防御素2和schlafen-2基因的表达及其信号转导  

Induction of β defensin-2 and schlafen-2 in L929 cells stimulated by LPS and its signaling pathways

作　　者：张妮[1] 房晓楠[1] 崔南[1] 陈新年[1] 

机构地区：[1]甘肃省新药临床前研究重点实验室兰州大学基础医学院病理生理学研究所,兰州730000

出　　处：《中国免疫学杂志》2010年第9期778-782,共5页Chinese Journal of Immunology

基　　金：甘肃省新药临床前研究重点实验室开放基金(GSKFKT-0703);国家大学生创新性试验计划(081073019)项目

摘　　要：目的:通过研究LPS对于小鼠成纤维细胞(L929)β防御素(defb)和schlafen(slfn)基因表达的影响及其信号转导通路,探讨纤维细胞对病原微生物的防御作用。方法:LPS(200ng/ml)处理L929细胞2、4、6小时,提取细胞总RNA,用RT-PCR和荧光定量PCR的方法检测defb1,2和slfn1,2,3基因表达;应用Westernblot的方法检测了defb2蛋白的表达。NF-κB和P38MAPK两种信号转导通路的化学抑制剂BMS345541和PD169316检测defb2和slfn2基因表达的信号转导通路。结果:LPS能诱导小鼠成纤维细胞defb2的表达,并增强slfn2的表达;P38MAPK和NF-κB信号转导通路调控小鼠成纤维细胞defb2和slfn2的表达。结论:在感染时,小鼠成纤维细胞可能通过诱导defb2的产生而发挥抵御病原微生物的作用。Objective：By studying the contribution of LPS to the expression of β-defensin（defb） and schlafen（slfn） in mouse fibroblast cells（L929） and the signal pathways,to explore the prevention of the fibroblast cells from pathogenic microorganisms.Methods：By exposure of L929 cells to LPS（200 ng/ml） for 2 h,4 h,6 h,total RNA were extracted,RT-PCR and quantitative real-time PCR assays were performed with specific primers for defb1,or 2 and slfn1,2 or 3;The expression of defb2 protein was verified by Western blot.BMS345541 and PD169316,two chemical inhibitors of NF-κB and P38MAPK signal pathways,were used to study the signal pathways for the induced defb2 and up-regulation of slfn2.Results：Exposure of L929 cells to LPS induced the activation of defb2 and up-regulated slfn2 genes expressions,and slfn2 and defb2 gene expressions were regulated by the NF-κB and P38MAPK signal pathways.Conclusion：In inflammation,mouse fibroblast cells may play a role against the pathogenic microorganisms by the activation of defb2.

关 键 词：LPS 小鼠β防御素2 小鼠schlafen 成纤维细胞 信号转导 

分 类 号：R392.12[医药卫生—免疫学]