Fasudil通过TLR4通路抑制脂多糖诱导的小鼠BV-2小胶质细胞TNF-α和IL-1β的表达  

Inhibition of Fasudil on lipopolysaccharide-induced TNF-α and IL-1β expressions through TLR4 pathway in murine BV-2 cells in vitro

作　　者：李艳花[1] 杨兴旺[2] 张辉[1] 尉杰忠[1] 刘春云[1] 丰玲[1] 李俊莲[2] 肖保国[3] 马存根[1,2] 

机构地区：[1]山西大同大学脑科学研究所,山西大同037009 [2]山西中医学院第三中医院脑病科,卫生部临床重点专科,山西太原030024 [3]复旦大学华山医院神经病学研究所,上海200025

出　　处：《细胞与分子免疫学杂志》2014年第1期11-14,共4页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金(81070957);山西省青年自然科学基金(2012021034-2);山西大同大学博士科研启动经费(2011-B-11);山西大同大学研究所科研项目启动经费(2006年)

摘　　要：目的探讨Fasudil对脂多糖(LPS)诱导BV-2小胶质细胞系促炎细胞因子表达中的作用。方法体外培养BV-2小胶质细胞系,实验分为PBS对照组、LPS刺激组、LPS联合Fasudil干预组,ELISA检测细胞TNF-α、IL-1β的释放,Griess法检测NO释放水平,流式细胞术检测Toll样受体4(TLR4)、TLR2蛋白表达。结果 LPS刺激BV-2细胞可导致TNF-α、IL-1β和NO的释放明显增加,还可导致炎性信号通路中的受体TLR4表达明显增加。Fasudil能明显抑制炎性因子的释放和TLR4的表达。结论 Fasudil可抑制LPS诱导的小胶质细胞NO、TNF-α和IL-1β释放,其作用机制可能与Fasudil下调TLR4通路有关。Objective To evaluate the effects of Fasudil on the production of proinflammatory cytokines in lipopolysaccharide （LPS）-stimulated BV-2 microglia cells. Methods The BV-2 cells cultured in vitro were divided into PBS control group, LPS stimulation group and LPS plus Fasudil group. The production of TNF-α and IL-1 was measured by ELISA. The release of NO was checked by Griess reagent assay, Toll-like receptor 2 （TLR2） and TLPA expressions were determined by flow cytometry. Results The stimulation of LPS significantly increased the production of TNF-α, IL-1β and NO as well as TLR4 protein expression in BV-2 cells. Fasudil attenuated NO production, and reduced the release of TNF-α and IL-1β in LPS- stimulated BV-2 cells. Interestingly, Fasudil also decreased TLPA expression. Conclusion Fasudil can suppress the production of TNF-α, IL-1β and NO of microglia cells induced by LPS, which may be associated with the down-regulation of TLR4 pathway.

关 键 词：脂多糖 BV-2小胶质细胞 TLR4受体 盐酸法舒地尔 

分 类 号：R392.11[医药卫生—免疫学] R446.61[医药卫生—基础医学]