Schisandrin A ameliorates MPTP-induced Parkinson’s disease in a mouse model via regulation of brain autophagy
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Schisandrin A (Sch A) is one of the principal bioactive lignans isolated from Fructus schisandrae. In this study, we demonstrated its protective effect and biochemical mechanism of action in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced mouse model of Parkinson’s disease. Sch A significantly ameliorated behavioural abnormalities and increased the number of nigral dopaminergic neurons detected by tyrosine hydroxylase immunohistochemistry. Pre-treatment with Sch A significantly decreased the levels of the inflammatory mediators IL-6, IL-1β, and TNF-α and markedly improved antioxidant defences by inhibiting the activity of MDA and increasing that of SOD. Furthermore, Sch A activated expression of the autophagy-related proteins LC3-II, beclin1, parkin, and PINK1 and increased mTOR expression. Taken together, these findings indicate that Sch A has neuroprotective effects against the development of Parkinson’s disease via regulation of brain autophagy.
KeywordsSchizandrin A Parkinson’s disease Autophagy LC3-II
This study was funded by Chinese Medicine Science and Technology Project of Zhejiang Province (Grant No. 20162097009594).
Compliance with ethical standards
Conflict of interest
The authors declare that they have no competing interests.
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