Rapamycin protects the mitochondria against oxidative stress and apoptosis in a rat model of Parkinson's disease

Jiang,Jianhua; Jiang,Juean; Zuo,Yuanyi; Gu,Zhenlun

doi:10.3892/ijmm.2013.1280

Rapamycin protects the mitochondria against oxidative stress and apoptosis in a rat model of Parkinson's disease

Authors:
- Jianhua Jiang
- Juean Jiang
- Yuanyi Zuo
- Zhenlun Gu
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Affiliations: Department of Pharmacology, Medical College of Soochow University, Suzhou Institute of Chinese Materia Medica, Suzhou 215007, P.R. China, Department of Special Requirements Ward, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China
Published online on: February 20, 2013 https://doi.org/10.3892/ijmm.2013.1280
Pages: 825-832

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Abstract

Parkinson's disease (PD) is a neurodegenerative disease, in which oxidative stress and mitochondrial dysfunction are responsible for neuronal apoptosis. Rapamycin plays a crucial role in reducing oxidative stress and protecting the mitochondria. However, its protective role in PD has not yet been fully elucidated. In this study, we report that pre-treatment with rapamycin provides behavioral improvements, protects against the loss of dopaminergic neurons, and alleviates mitochondrial ultrastructural injuries in a rat model of PD. Peroxide levels were lower and antioxidant activities were higher in PD rats pre-treated with rapamycin compared to the PD rats pre-treated with the vehicle. Furthermore, pre-treatment with rapamycin significantly elevated the expression of anti-apoptotic markers and reduced the levels of pro-apoptotic markers compared to pre-treatment with the vehicle. In conclusion, our results demonstrated that rapamycin reduced oxidative stress and alleviated mitochondrial injuries in the 6-hydroxydopamine (6-OHDA)-induced rat model of PD, which may subsequently contribute to its anti-apoptotic effects. The ability of rapamycin to exhibit neuroprotection in a rat model of PD may be related to its antioxidant capabilities.

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