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Parkinson Disease: HELP
Articles by Wen-Juan Zhao
Based on 1 article published since 2010
(Why 1 article?)

Between 2010 and 2020, Wen-Juan Zhao wrote the following article about Parkinson Disease.
+ Citations + Abstracts
1 Article Resveratrol alleviates MPTP-induced motor impairments and pathological changes by autophagic degradation of α-synuclein via SIRT1-deacetylated LC3. 2016

Guo, Yan-Jie / Dong, Su-Yan / Cui, Xin-Xin / Feng, Ya / Liu, Te / Yin, Ming / Kuo, Sheng-Han / Tan, Eng-King / Zhao, Wen-Juan / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. · Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, , Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China. · School of Pharmacy, Shanghai Jiao Tong University, Shanghai, P.R. China. · Department of Neurology, College of Physicians and Surgeons, Columbia University, NY, USA. · Department of Neurology, Singapore General Hospital, National Neuroscience Institute, Singapore. · Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. yunchw@medmail.com.cn. ·Mol Nutr Food Res · Pubmed #27296520.

ABSTRACT: SCOPE: The accumulation of misfolded α-synuclein in dopaminergic neurons is the leading cause of Parkinson's disease (PD). Resveratrol (RV), a polyphenolic compound derived from grapes and red wine, exerts a wide range of beneficial effects via activation of sirtuin 1 (SIRT1) and induction of vitagenes. Here, we assessed the role of RV in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) induced mouse model of PD and explored its potential mechanisms. METHODS AND RESULTS: RV and EX527, a specific inhibitor of SIRT1, were administered before and after MPTP treatment. RV protected against MPTP-induced loss of dopaminergic neurons, and decreases in tyrosine hydroxylase and dopamine levels, as well as behavioral impairments. Meanwhile, RV administration activated SIRT1. Microtubule-associated protein 1 light chain 3 (LC3) was then deacetylated and redistributed from the nucleus to the cytoplasm, which provoked the autophagic degradation of α-synuclein in dopaminergic neurons. Furthermore, EX527 antagonized the neuroprotective effects of RV by reducing LC3 deacetylation and subsequent autophagic degradation of α-synuclein. CONCLUSION: We showed that RV ameliorated both motor deficits and pathological changes in MPTP-treated mice via activation of SIRT1 and subsequent LC3 deacetylation-mediated autophagic degradation of α-synuclein. Our observations suggest that RV may be a potential prophylactic and/or therapeutic agent for PD.