【摘要】 目的:研究细胞外信号调节激酶对氧糖剥夺(oxygen-glucose deprivation,OGD)后大鼠海马神经元的作用。方法:建立培养乳鼠海马神经元OGD模型,并分为正常对照组、OGD组、PD 98059 10μmol/L、30μmol/L组。流式细胞仪Annexin V/PI双染色法检测神经元细胞凋亡率,Western blot法检测ERK1/2、pERK1/2的表达。结果:与正常对照组相比,OGD组神经元的凋亡率升高(P<0.01),pERK1/2的表达降低(P<0.01),与OGD组相比,PD98059组神经元凋亡率明显升高(P<0.01),pERK1/2的表达明显降低(P<0.01),30μmol/L组较10μmol/L组凋亡率升高及pERK1/2表达降低更为显著(P<0.01),各组ERK含量无明显变化(P>0.05)。结论:ERK可能参与氧糖剥夺后的神经元凋亡,抑制ERK通路可促进神经元凋亡。更多还原

【Abstract】 Objective: To investigate the effect of excelluar signal-regulated kinase(ERK) on rat hippocampal neurons with oxygen-glucose deprivation(OGD).Methods:Cultured hippocampal neurons were designed into four groups:normal group,OGD group,PD98059 10 μmol/L and 30 μmol/L groups.The apoptosis of neurons was determined by flow cytometry,and Western blot was used to evaluate protein expression of ERK1/2 and pERK1/2.Results:Compared with normal control group,neuron apoptosis increased while pERK1/2 protein expression decreased obviously in OGD group(both P < 0.01).Neuron apoptosis increased and pERK1/2 protein expression decreased more significantly in PD98059 groups compared with OGD group(both P < 0.01).Changes in 30 μmol/L PD98059 group were more significant than 10 μmol/L PD98059 group(P < 0.01).Each group showed no significant change in ERK expression(P > 0.05).Conclusion:ERK may be involved in neuronal apoptosis after OGD,and inhibition of ERK pathway can promote neuronal apoptosis.更多还原