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目的探讨低剂量鱼藤酮对乳鼠中脑黑质脑片多巴胺能神经元的毒性作用及依达拉奉的保护作用。方法取Wistar乳鼠中脑黑质脑片进行培养,酪氨酸羟化酶(TH)免疫组化染色观察多巴胺神经元毁损情况,western-blot测定各组脑片α-突触核蛋白(α-Synuclein)含量,扫描电镜观察脑片超微病理结构变化。结果黑质脑片多巴胺神经元的数目随鱼藤酮浓度及培养时间的增加而明显减少,多巴胺神经元的超微病理显示氧化应激性损害,α-Synuclein的含量随鱼藤酮浓度的增加而升高,依达拉奉+鱼藤酮组较鱼藤酮组能够减少多巴胺能神经元的凋亡并使α-Synuclein的表达量减少。结论成功利用黑质脑片器官型培养体系建立了帕金森病(Pakinson’s disease)模型;低剂量鱼藤酮导致选择性多巴胺神经元的凋亡,并导致α-Synuclein的含量增加,自由基清除剂依达拉奉对此有保护作用。
Objective To investigate the toxic effects of low dose rotenone on dopaminergic neurons in substantia nigra brain slices of neonatal rats and the protective effect of edaravone. Methods Wistar rats were cultured in substantia nigra brain slices and the damage of dopaminergic neurons was observed by tyrosine hydroxylase (TH) immunohistochemical staining. The α-synuclein (α Synuclein) content, scanning electron microscopy observation of ultrastructural changes in brain slices. Results The number of dopamine neurons in substantia nigra brain decreased with the increase of rotenone concentration and culture time. The ultrastructural changes of dopamine neurons showed oxidative stress damage. The content of α-Synuclein increased with the increase of rotenone concentration, Edaravone + rotenone group compared with rotenone group can reduce the apoptosis of dopaminergic neurons and reduce the expression of α-Synuclein. Conclusions Pakinson’s disease model was successfully established by using organotypic culture system of the substantia nigra. The low dose of rotenone resulted in the apoptosis of selective dopamine neurons and resulted in the increase of the content of α-Synuclein. The scavenger of radical scavenger Lam Fong has a protective effect on this.