PI3K/AKT途径在大肠埃希菌诱导U937细胞凋亡中的作用  

ROLE OF PI3K/AKT IN THE SIGNAL TRANSDUCTION OF APOPTOSIS OF U937 CELL LINES INDUCED BY E. COLI

作　　者：王佳贺[1] 阚亮[1] 舒林华[2] 杨艳敏[1] 何平[1] 

机构地区：[1]中国医科大学附属盛京医院老年病科,沈阳110004 [2]中国医科大学附属盛京医院儿科,沈阳110004

出　　处：《中国组织化学与细胞化学杂志》2009年第4期377-380,共4页Chinese Journal of Histochemistry and Cytochemistry

基　　金：辽宁省高等学校科研项目计划(2008771);辽宁省博士科研启动基金(20081055)

摘　　要：目的探讨PI3K/AKT信号转导通路在大肠埃希菌(Escherichia coli,E.coli)诱导的人巨噬细胞系U937细胞凋亡中的作用。方法利用Western blot分析检测E.coli感染不同时间后磷酸化及非磷酸化AKT的表达;预先用不同浓度的LY294002(PI3K途径抑制剂)处理U937细胞60min,观察E.coli感染30min后U937细胞的凋亡情况。结果随着感染时间的延长,磷酸化AKT的表达逐渐下降。加入PI3K的抑制剂LY294002后,U937细胞的凋亡率逐渐升高。结论PI3K/AKT信号转导通路参与了E. coli诱导的U937细胞凋亡过程。LY294002通过特异性地抑制PI3K/AKT活性增加E.coli诱导的U937细胞凋亡率。Objective To investigate the role of the phosphatidylinositol 3 kinase （PI3K） pathway in the apoptosis of U937 cells induced by E. coll. Methods The U937 cell lines were treated with E. coli for different durations. AKT activity was detected by Western blot. In some experiments, U937 cells were pretreated with LY294002 （an inhibitor for PI3K pathway）, and the apoptosis rate of U937 cells were detected. Results The downregulation of AKT by E. coli was statistically significant and the inhibition of PI3K with LY294002 caused further increase in apoptosis of U937 cells. Conclusion The signaling pathway PI3K/AKT participates in the apoptosis of U937 cells. LY294002 increases U937 cell apoptosis induced by E. coli by inhibiting the activity of PI3K/AKT.

关 键 词：大肠埃希菌 细胞凋亡 U937 磷脂酰肌醇-3激酶 AKT 

分 类 号：R378.2[医药卫生—病原生物学]