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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2010年第11期2161-2164,共4页
Chinese Journal of Pathophysiology
关键词
脂联素
心肌细胞
过氧化氢
细胞凋亡
Adiponectin Cardiomyocytes Hydrogen peroxide Apoptosis
