GDNF和HSV-GDNF对培养的大鼠脊髓运动神经元缺氧后的Bcl-2表达的影响

目的:观察细胞胶质源性神经营养因子(Glial cell line-derived neurotrophic factor,GDNF)和单纯疱疹病毒介导的GDNF(GDNF transformed by herpes simplex virus vector,HSV-GDNF)对体外培养的大鼠脊髓运动神经元缺氧-复氧时的作用和Bcl-2表达的影响。方法:观察缺氧2h、4h和缺氧4h后恢复供氧24、72h时,脊髓运动神经元存活数,并用抗Bcl-2抗血清行免疫组织化学染色,对Bcl-2免疫反应阳性神经元作平均光密度分析。结果:经GDNf、HSV-GDNF孵育的脊髓运动神经元缺氧-复氧后Bcl-2表达较对照组明显增强,神经元损伤程度减轻,神经元存活数明显高于对照组,且HSV-GDNF组的效果更好。结论:GDNF、HSV-GDNF对缺氧-复氧的大鼠脊髓运动神经元有保护作用,HSV-GDNF比GDNF更能增强缺氧-复氧后脊髓运动神经元Bcl-2的表达,提高神经元存活数,抑制缺氧后神经元的死亡。

Effects of GDNF and HSV-GDNF on Bcl-2 expression of rat spinal cord motoneurons after anoxia

Objective:To study the effects of GDNF and HSV-GDNF on Bcl-2 expression of rat spinal cord motoneurons after anoxic-reoxygenation in vitro. Methods:Spinal cord motoneurons were immunohistochemically stained by the anti-serum of Bcl-2 after anoxia for 2 and 4 h and reoxygenation for 24 and 72 h. The number of the living neurons and the mean optical densities of Bcl-2 immunoreactive positive neurons were observed. Results:After anoxia the number of the living neurons and mean optical density of Bcl-2 immunoreactive motoneurons were significantly increased in GDNF and HSV-GDNF groups,compared with that of control,and effects of HSV-GDNF were better than the that of GDNF. Conclusion:GDNF and HSV-GDNF can increase Bcl-2 expression and decrease the death of cultured motoneurons after anoxi-a. HSV-GDNF may better protect motoneurons from the damage induced by anoxia than GDNF.