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目的:研究依达拉奉及帕吉林对鱼藤酮诱导的帕金森病(PD)大鼠模型的保护作用及机制。方法:60只5周龄♂Wistar大鼠随机分为4组,即鱼藤酮处理组、依达拉奉组、帕吉林组及对照组。分别给予鱼藤酮、鱼藤酮+依达拉奉、鱼藤酮+帕吉林和大豆油连续皮下注射8周。造模结束后处死动物游离中脑,进行免疫组织化学分析及电镜观察,并用流式细胞仪检测细胞内活性氧簇(ROS)的变化及线粒体膜电位改变。结果:相对于对照组,鱼藤酮组大鼠中脑神经元内ROS表达上升、线粒体膜电位严重降低(P<0.01);依达拉奉处理可以减缓鱼藤酮诱导的ROS的产生及线粒体膜电位的下降,并上调抗凋亡蛋白Bcl-2、Bcl-XL的表达,动物也未出现明显的PD症状;帕吉林组大鼠中脑神经元内ROS产生仍较高,虽然线粒体膜电位下降有所缓解,但大鼠仍表现出PD的行为学特征。结论:依达拉奉可能通过减少鱼藤酮诱导的ROS产生而对PD大鼠发挥神经保护作用。而帕吉林的保护作用并不明显,虽然可部分减少中脑神经元线粒体膜电位的下降,但仍不足以防止PD症状的出现。
Objective: To study the protective effect and mechanism of edaravone and perindoline on rotenone-induced Parkinson’s disease (PD) rats. Methods: Sixty male Wistar rats of 5 weeks old were randomly divided into 4 groups: rotenone group, edaravone group, pargyline group and control group. Rotenone, rotenone + edaravone, rotenone + perindoline and soybean oil were injected subcutaneously for 8 weeks. After modeling, the free midbrain was sacrificed and immunohistochemistry and electron microscopy were performed. Changes of intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by flow cytometry. Results: Compared with the control group, the ROS expression in the midbrain neurons of rotenone group increased and the mitochondrial membrane potential was significantly decreased (P <0.01). Edaravone treatment attenuated the production of rotenone-induced ROS and mitochondrial membrane potential , And up-regulated the expression of anti-apoptotic proteins Bcl-2 and Bcl-XL, but no obvious PD symptoms were observed in animals. The production of ROS in midbrain neurons of pargyline group was still high, although mitochondrial membrane potential decreased , But rats still exhibit behavioral characteristics of PD. Conclusion: Edaravone may play a neuroprotective role in PD rats by reducing rotenone-induced ROS production. However, the protective effect of perindoline is not obvious. Although it can partially reduce the mitochondrial membrane potential of the midbrain neurons, it is still not enough to prevent the occurrence of PD symptoms.