摘要
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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2010年第9期1704-1707,共4页
Chinese Journal of Pathophysiology