姜黄素经JAK2/STAT3通路抑制小胶质细胞活化的实验研究  

Curcumin inhibits activated microglia via JAK2/STAT3 pathway

作　　者：祖佳宁[1] 庄金鹏[1] 闫景龙[1] 徐公平[1] 夏景君[1] 张志鹏[1] 

机构地区：[1]哈尔滨医科大学附属第二医院骨七科,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2017年第2期109-112,共4页Journal of Harbin Medical University

基　　金：黑龙江省中医药科研项目(2HY16-053)

摘　　要：目的探讨姜黄素在脂多糖(lipopolysaccharide,LPS)作用下对小胶质细胞系BV2细胞活化抑制的可能作用机制。方法常规培养细胞,用LPS及不同浓度的姜黄素(curcumin,CUR)处理24 h,ELISA检测各组细胞上清LDH、TNF-α、IL-1β和IL-6的浓度;Western blot检测P-STAT3(Tyr705)、STAT3、P-JAK2(Tyr1007/1008)和JAK2表达水平。结果与对照组相比,LPS组BV2细胞上清中LDH、TNF-α、IL-1β和IL-6含量增多(P<0.01),P-STAT3和P-JAK2水平增高(P<0.05);与LPS组相比姜黄素各组降低了BV2细胞上清中LDH、TNF-α、IL-1β和IL-6含量(P<0.01),降低了P-STAT3和P-JAK2水平(P<0.05)。结论姜黄素经JAK2/STAT3信号通路抑制小胶质细胞的活化,且呈剂量依赖性。Objective To investigate the mechanism of curcumin inhibiting LPS-activated mieroglia （BV2）. Methods BV2 cells were cultured regulary, and then treated with LPS and curcumin at different concentrations for 24 h. The cells and cultured supernatant were harvested for detection of LDH, TNF-α, IL-1β and IL-6 by ELISA, P-STAT3 （TyrT05） and STAT3, P- JAK2 （Tyr1007/1008） and JAK2 by immunofluoreseence assay and Western blot. Results Compared with control group, the levels of LDH, TNF-α, IL-1β, IL-6, P-STAT3 and P-JAK2 were higher in LPS-aetivated group （P 〈 0. 05 ）. Compared with LPS-activated group, the levels of LDH, TNF-α, IL-1β, IL-6, P-STAT3 and P-JAK2 were decreased in eurcumin groups （P 〈 0. 05 ）. Conclusion Curcumin can inhibit LPS-aetivated mieroglia via JAK2/STAT3 pathway.

关 键 词：姜黄素 小胶质细胞 活化 JAK2/STAT3通路 

分 类 号：R743.34[医药卫生—神经病学与精神病学]