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目的 :研究自由基、神经营养因子及细胞凋亡在帕金森病发病中的变化。方法 :通过脑立体定向注射 6 羟基多巴胺的方法建立大鼠PD模型 ,采用TUNEL法 ,免疫组化技术 ,生化方法 ,观察大鼠黑质细胞凋亡数量 ,纹状体多巴胺含量 ,脑胶质源性神经营养因子 (GDNF)表达及自由基和抗自由基酶的变化。结果 :PD大鼠黑质存在明显的细胞凋亡 ,自由基反应增强 ,抗自由基酶和纹状体多巴胺含量及GDNF减少 ,与对照组存在显著性差异 ( P <0 0 5 )。结论 :自由基反应增强 ,营养因子缺乏及细胞凋亡参与了PD的发病 ,可能是其发病机制之一
Objective: To study the changes of free radicals, neurotrophic factors and apoptosis in the pathogenesis of Parkinson’s disease. Methods: PD model was established by injection of 6-hydroxydopamine into brain. The TUNEL, immunohistochemistry and biochemical methods were used to observe the number of apoptotic cells in substantia nigra of striatum, striatum dopamine content, Expression of GDNF and the Changes of Free Radical and Free Radical Enzymes. Results: There was obvious apoptosis in the substantia nigra of PD rats, the radical reaction was enhanced, the content of dopamine and GDNF in free radical enzyme and striatum was decreased, which was significantly different from the control group (P <0.05). Conclusion: Increased free radical response, lack of nutrition factors and apoptosis are involved in the pathogenesis of PD, which may be one of the pathogenesis