高糖应激对H9c2细胞凋亡作用  

influence of high glucose-induced stress on the survival of H9c2 cells

作　　者：赖滨[1] 蔡金梅[1] 董靖德[2] 

机构地区：[1]南京医科大学第一附属医院老年内分泌病科,210029 [2]南京医科大学附属脑科医院

出　　处：《江苏医药》2009年第12期1476-1478,共3页Jiangsu Medical Journal

摘　　要：目的探讨高糖应激早期对H9c2细胞存活的影响及其可能的信号转导通路。方法高糖培养H9c2细胞24 h后,收集细胞进行细胞活力和凋亡的测定,用Western blot方法测定蛋白激酶(Akt)的磷酸化水平和内皮细胞一氧化氮合酶(eNOS)的表达。结果与对照(NG)组相比,高糖培养(HG)组H9c2细胞活力改善,凋亡减少,而PI3K抑制剂LY294002预处理和NOS抑制剂L-NAME预处理均抑制短期高糖培养对H9c2细胞的保护作用。与NG组相比,HG组早期Akt磷酸化水平升高,eNOS蛋白表达增加,结论在高糖应激早期(24 h内),高糖通过活化PI3K/Akt/eNOS信号通路,改善H9c2细胞的活力,减少其凋亡。Objective To investigate the potential influence of high glucose on the survival of H9c2 cells and posible signaling pathways. Methods After the H9c2 cells were cultured for 24 hours in the high glucose condition,the cells were collected for determining the cell viability and apoptosis. The phosphorylation of Akt and expression of eNOS were measured by Western blot. Results High glucose improved the viability of H9c2 cells and reduced their apoptosis. High glucose increased the phosphorylation of Akt followed by increased eNOS expression. The PI3K inhibitor LY294002 abolished the protective effect of high glucose on H9c2 cells as well as the NOS inhibitor L-NAME. Conclusion In the early phase,high glucose protects the H9c2 cells from apoptosis through activating PI3K/Akt/eNOS signaling pathway.

关 键 词：H9C2细胞 凋亡 蛋白激酶 内皮细胞一氧化氮合酶 

分 类 号：R587[医药卫生—内分泌]