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Autophagy-related protein expression in the substantia nigra and eldepryl intervention in rat models of Parkinson's disease

机译：黑质和eldepryl干预大鼠帕金森病模型中的自噬相关蛋白表达

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Autophagy has been shown to participate in the pathogenesis of Parkinson's disease (PD), but its precise mechanism remains poorly understood. This study observed autophagy, autophagy-related protein Beclin1 and microtubule-associated protein 1 light chain 3 (LC3) expression in substantia nigra, and eldepryl effects on their expression, as well as explored autophagy effects on the onset of PD and the mechanism of action of eldepryl on PD in rat models. Models of PD were established by subcutaneous injection of rotenone through back of the neck. Results indicated that Beclin1, LC3 protein expression and LC3II/LC3I ratio were higher in substantia nigra of rats in the model group compared with the control group. Beclin1, LC3 protein expression and LC3II/LC3I ratio were higher at 8 days than that at 4 days in the model group, showing significant differences. Beclin1, LC3 protein expression and LC3II/LC3I ratio were lower in the rat substantia nigra of the eldepryl group than in the model group. Beclin1, LC3 protein expression and LC3II/LC3I ratio were lower at 8 days than at 4 days in the eldepryl group, showing significant differences. Results suggested that autophagy plays a key role in the onset of PD. Eldepryl exerts therapeutic effects on PD by inhibiting autophagy of nerve cells in substantia nigra of rat models of PD. (C) 2015 Elsevier B.V. All rights reserved.
机译：自噬已被证明参与帕金森氏病（PD）的发病机制，但其确切的机制仍知之甚少。这项研究观察了黑质中自噬，自噬相关蛋白Beclin1和微管相关蛋白1轻链3（LC3）的表达以及eldepryl对它们的表达的影响，并探讨了自噬对PD发作和作用机理的影响。地普利对大鼠模型PD的影响PD的模型是通过从脖子后部皮下注射鱼藤酮来建立的。结果表明，模型组大鼠黑质中Beclin1，LC3蛋白表达和LC3II / LC3I比值均高于对照组。模型组Beclin1，LC3蛋白表达和LC3II / LC3I比值在第8天高于第4天，显示出显着差异。 Eldepryl组的大鼠黑质中的Beclin1，LC3蛋白表达和LC3II / LC3I比均低于模型组。 Eldepryl组的Beclin1，LC3蛋白表达和LC3II / LC3I比在第8天低于在第4天，显示出显着差异。结果表明自噬在PD的发作中起关键作用。 Eldepryl通过抑制PD模型大鼠黑质中神经细胞的自噬而对PD产生治疗作用。 （C）2015 Elsevier B.V.保留所有权利。

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