瘦素抑制H_2O_2诱导的大鼠心肌细胞凋亡

Leptin protects rat cardiomyocytes from H_2O_2-induced apoptosis

目的:观察瘦素(leptin)对H2O2诱导的大鼠心肌细胞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)法观察瘦素对H2O2诱导的大鼠心肌细胞H9c2凋亡的影响;应用Western blotting法观察瘦素、H2O2对caspase-3、胞外信号调控激酶(ERK)活性的影响。结果:(1)瘦素对H2O2诱导的H9c2细胞凋亡具有显著的抑制作用(与对照组比较P<0.01),该作用可被ERK激酶抑制剂PD98059所阻断。(2)H2O2明显抑制ERK活性;而瘦素可激活ERK并部分阻断H2O2诱导的caspase-3激活。结论:瘦素对H2O2诱导的H9c2细胞凋亡具有抑制作用,其机制可能与其激活ERK信号途径有关。

AIM： To investigate the effect of leptin on H2O2-induced apoptosis in rat cardiomyocytes （ H9c2 cells） and the underlying mechanisms. METHODS： Terminal-deoxynucleotidyl transferase mediated nick end labeling （ TUNEL） was used to determine H2O2-induced apoptosis in H9c2 cells in the absence or presence of leptin. The activities of caspase-3 and extracellular signal-regulated kinase （ ERK） were examined by Western blotting. RESULTS： （ 1） Leptin significantly inhibited H2O2-induced apoptosis in H9c2 cells （ P 0. 01） . This effect of leptin was opposed by MEK inhibitor PD98059. （ 2） H2O2 inhibited basal ERK activity. Leptin activated ERK and partially inhibited H2O2-induced caspase-3 activation. CONCLUSION： Leptin protects H9c2 cells from H2O2-induced apoptosis possibly by activating ERK.