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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。
AIM: To investigate the effect of extracellular signal-regulated kinase on hippocampal neurons in rats after oxygen-glucose deprivation (OGD). Methods: The cultured OGD model of cultured hippocampal neurons was established and divided into normal control group, OGD group, PD 98059 10μmol / L, 30μmol / L group. The apoptosis rate of neurons was detected by flow cytometry Annexin V / PI double staining and the expression of ERK1 / 2 and pERK1 / 2 was detected by Western blot. Results: Compared with the normal control group, the apoptosis rate of neurons in OGD group was significantly increased (P <0.01) and the expression of pERK1 / 2 was decreased (P <0.01). Compared with OGD group, the apoptosis rate of neurons in PD98059 group (P <0.01). The apoptosis rate and the expression of pERK1 / 2 in 30μmol / L group were significantly higher than those in 10μmol / L group (P <0.01) There was no significant change in ERK content in all groups (P> 0.05). Conclusion: ERK may be involved in neuronal apoptosis after oxygen deprivation, and inhibition of ERK pathway may promote neuronal apoptosis.