脂联素激活AKT抑制H_2O_2诱导的大鼠心肌细胞凋亡  

Adiponectin activates AKT and protects rat cardiomyocytes against H_2O_2-induced apoptosis

作　　者：陈诗鸿[1] 倪一虹[1] 庄向华[1] 孙福敦[1] 潘喆[1] 李晓博[1] 姜冬青[1] 孙爱丽[1] 娄能俊[1] 刘元涛[1] 

机构地区：[1]山东大学第二医院内分泌科,山东济南250033

出　　处：《中国病理生理杂志》2010年第11期2161-2164,共4页Chinese Journal of Pathophysiology

摘　　要：目的:观察脂联素(adiponectin)对H2O2诱导的大鼠心肌细胞(H9c2)凋亡的影响并探讨其作用机制。方法:应用脱氧三磷酸尿苷缺口末端标记(TUNEL)法观察脂联素对H2O2诱导的H9c2细胞凋亡的影响;应用Western blotting法观察脂联素对Akt和caspase-3活性的影响。结果:脂联素对H2O2诱导的H9c2细胞凋亡具有显著的抑制作用(P<0.01)。脂联素直接激活Akt并增加了H2O2诱导的Akt活性,对H2O2诱导的caspase-3激活有显著抑制作用(P<0.01)。Akt上游激酶PI3K的特异抑制剂LY294002不但增加了H2O2诱导的H9c2细胞凋亡率,而且消除了脂联素的抗凋亡作用。结论:脂联素对H2O2诱导的H9c2细胞凋亡具有抑制作用,其机制可能与其激活PI3K/Akt通路、抑制caspase凋亡信号通路有关。AIM： To study the effect of adiponectin on H2O2-induced apoptosis in rat cardiomyocytes （H9c2 cells）. METHODS： Terminal deoxynucleotidyl transferase-mediated nick end labeling （TUNEL） was used to determine H2O2-induced apoptosis of H9c2 cells in the absence or presence of adiponectin. The content of caspase-3 and Akt （protein kinase B, PKB） was examined by Western blotting. RESULTS： Adiponectin significantly inhibited H2O2-induced apoptosis in H9c2 cells （P〈0.01）. Adiponectin increased basal and H2O2-induced Akt activity and significantly inhibited H2O2-induced activation of caspase-3 （P〈0.01）. Pretreatment with LY294002, a specific inhibitor of Akt upstream kinase PI3K （phosphatidylinositol 3-kinase）, not only increased H2O2-induced H9c2 cell apoptosis, but also abrogated the anti-apoptotic effect of adiponectin. CONCLUSION： Adiponectin protects H9c2 cells against H2O2-induced apoptosis by activating PI3K/Akt signaling pathway.

关 键 词：脂联素 心肌细胞 过氧化氢 细胞凋亡 

分 类 号：R34[医药卫生—基础医学]