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目的探讨甘氨酸对氧糖剥夺诱导神经元损伤的作用及机制。方法采用体外培养的大鼠原代神经元建立氧糖剥夺模型,随机分为正常对照组、氧糖剥夺组和甘氨酸处理组,应用MTT、流式细胞术等方法检测甘氨酸对神经元活性、生存率、细胞凋亡的影响;应用蛋白质印迹测定甘氨酸对凋亡蛋白Bcl-2、Bcl-xL、Bad、Bax的影响。结果甘氨酸能够提高大鼠原代神经元活力和存活率,减少细胞凋亡,并且能够增加抗凋亡因子Bcl-2,降低促凋亡因子Bax的表达(P<0.05或P<0.01)。结论甘氨酸对氧糖剥夺神经元有明显的保护作用,该作用可能与促进抗凋亡因子、抑制促凋亡因子释放有关。
Objective To investigate the effect and mechanism of glycine on neuronal injury induced by oxygen sugar deprivation. Methods Oxygen-glucose deprivation model was established by primary rat neurons cultured in vitro and randomly divided into normal control group, OGD group and glycine treatment group. MTT and flow cytometry were used to detect the effects of glycine on neuronal activity, survival The effects of glycine on apoptosis proteins Bcl-2, Bcl-xL, Bad and Bax were determined by Western blotting. Results Glycine increased the viability and survival rate of primary neurons in rats, decreased apoptosis, increased the expression of anti-apoptotic factor Bcl-2 and decreased the expression of pro-apoptotic factor Bax (P <0.05 or P <0.01). Conclusion Glycine has a significant protective effect on oxygen-deprived neurons. This effect may be related to promoting anti-apoptotic factors and inhibiting the release of pro-apoptotic factors.