• Lei Wang, Xinghong Wu, Ge Yang, Nan Hu, Zijian Zhao, Lei Zhao, and Shengyu Li.
• Institute of Agro-food Technology, Jilin Academy of Agricultural Sciences, Changchun 130033, PR China; School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun 130117, PR China; School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, PR China.
• Neuroscience. 2022 Aug 21; 498: 64-72.

AbstractParkinson's disease (PD) is a complex and multifactorial neurodegenerative disease. The main pathological feature of PD is the loss or apoptosis of dopaminergic neurons in the substantia nigra (SN). This study aimed to investigate the protective effect of cannabidiol (CBD) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neuronal dopamine injury by inhibiting neuroinflammation, which was one of the factors that cause neuronal apoptosis. Male SPF C57BL/6 mice were used to create a PD model by administering MPTP intraperitoneally for seven days and treated by oral administration of CBD for 14 days. Behaviorally, CBD improved cognitive dysfunction and increased the number of spontaneous locomotion in PD mice. Biochemically, CBD increased the levels of 5-HT, DA and IL-10, and decreased the contents of TNF-α, IL-1β and IL-6. Pathologically, CBD increased the expression of tyrosine hydroxylase (TH). Mechanistically, CBD up-regulated the expression of Bcl-2, down-regulated the levels of Bax and Caspase-3, and repressed the expression of NLRP3/caspase-1/IL-1β inflammasome pathway. In summary, CBD has a therapeutic effect on MPTP-induced PD mice by inhibiting the apoptosis of dopaminergic neurons and neuroinflammation. Therefore, CBD is a potential candidate for PD therapy.Copyright © 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

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