中文摘要：

目的通过神经元氧糖剥夺模型研究Ⅰ组代谢型谷氨酸受体拮抗剂α-甲基-4-羧苯基甘氨酸（MCPG）对神经元损伤的保护作用,并初步探讨其机制。方法大鼠皮层神经元原代培养2w后,采用氧糖剥夺法建立损伤模型,通过乳酸脱氢酶（LDH）活性测定及碘化丙啶（PI）/Hoechst33342双染鉴定神经元损伤程度;加入Ⅰ组代谢型谷氨酸受体拮抗剂MCPG（1mmol/L）,通过脱氧核糖核苷酸末端转移酶介导的缺口末端标记法（TUNEL）检测神经元凋亡情况,并采用蛋白印迹法研究凋亡相关因子caspase-3、细胞外信号调节激酶1/2（ERK1/2）、磷酸化ERK1/2（p-ERK1/2）的表达变化,讨论MCPG抗凋亡作用与ERK1/2信号通路的关系。结果 MCPG能抑制ERK1/2信号通路的活化并降低凋亡相关因子caspase-3的表达,减轻氧糖剥夺造成的神经元凋亡。结论 MCPG能够通过ERK1/2信号通路减轻氧糖剥夺造成的神经元凋亡。

英文摘要：

Objective To investigate the neuroprotective effect of group Ⅰ metabotropic glutamate receptor antagonist α-methy-1,4-carboxyphenylglycine （MCPG） by using an oxygen glucose deprivation neuron model and its possible mechanism.Methods After cultured for 2 weeks in vitro,rat cortical neurons were exposed to oxygen glucose deprivation （OGD）.The cell viability was evaluated by the lactate dehydrogenase （LDH） activity and the immunofluorescence double staining of propidium iodide （PI） and Hoechst 33342.After treated with group Ⅰ metabotropic glutamate receptor antagonist MCPG （1 mmol/L）,the apoptosis of neurons was detected by the terminal deoxynucleotidyl transferase （TdT）-mediated dUTP biotin nick end-labeling （TUNEL） assay.The expressions of caspase-3,extracellular signal-regulated kinase （ERK）1/2 and phosphorylated ERK1/2 （p-ERK1/2） were measured to probe into the relationship between the anti-apoptotic effect of MCPG and ERK1/2 signaling pathway by Western blot.Results MCPG inhibited the activation of ERK1/2 and decreased the expression of apoptosis-related factor caspase-3.The apoptosis of neurons induced by OGD was reduced by the treatment of MCPG.Conclusion MCPG may attenuate the neuronal apoptosis induced by OGD by ERK1/2 pathway.