摘要
目的观察尼古丁在小胶质细胞炎性反应中的作用。方法将培养的小胶质细胞系(BV-2)分为6组:对照组、谷氨酸组、尼古丁组、谷氨酸+尼古丁组、谷氨酸+高浓度尼古丁组、谷氨酸+尼古丁+α-银环蛇毒素组,培养24h、48h,用ELISA法检测外源性尼古丁对TNF-α及IL-1β的作用。结果 (1)谷氨酸(浓度500μmol/L)使小胶质细胞表达TNF-α及IL-1β增多;(2)尼古丁(浓度10μmol/L)抑制小胶质细胞表达TNF-α及IL-1β;(3)加入α-银环蛇毒素后,α7-n AChR被阻断,尼古丁(浓度10μmol/L)使小胶质细胞表达TNF-α及IL-1β增多。结论 (1)谷氨酸可引发小胶质细胞释放炎性因子(TNF-α及IL-1β);(2)尼古丁抑制小胶质细胞释放炎性因子TNF-α及IL-1β;(3)尼古丁抑制作用是通过小胶质细胞膜上的α7-n AChR实现。
Objective To investigate the role of nicotine induced inflammatory response in microglia. Methods Different concentrations of nicotine( Ni) and glutamic acid( GLU) were added into the cultured microglia cell line( BV-2). They were divided into control group,glutamic acid group,nicotine group,glutamic acid plus nicotine group,glutamic acid plus high concentration nicotine group and glutamic acid plus nicotine group with α-bungarotoxin group. The cells were cultured for 24 h and 48 h. TNF-alpha and IL-1 beta were detected by ELISA fit,which were influenced by exogenous nicotine. Results( 1) glutamate( concentration 500μmol/L) increased the expression of TNF-alpha and IL-1 beta in microglia;( 2) nicotine( 10 μmol/L) inhibited the expression of TNF-alpha and IL-1 beta in microglia;( 3) After adding alpha bungarotoxin,alpha 7-n AChR was blocked,nicotine( concentration of 10 μmol/L) increased the expression of TNF-alpha and IL-1 beta in microglia. Conclusion( 1) glutamate can cause the release of inflammatory cytokines( TNF-alpha and IL-1 beta);( 2) Nicotine inhibits the expression of TNF-alpha and IL-1 beta in microglia;( 3) The inhibitory effect of nicotine is through the alpha 7-n AChR on the membrane of the microglia.
作者
崔小芬
李鑫鑫
张丽丽
王娜
关艳中
CUI Xiao -fen;et al(Mudanjiang Medical University, Mudanjiang 157011, China)
出处
《牡丹江医学院学报》
2018年第2期5-7,4,共4页
Journal of Mudanjiang Medical University
基金
国家自然科学基金(81371463)
黑龙江省自然科学基金(H2017076)
牡丹江医学院研究生创新科研项目(2016YJSCX-21MY
2017YJSCX-02MY
2017YJSCX-09MY)