Biomolecules & Therapeutics
Botulinum Toxin A Ameliorates Neuroinflammation in the MPTP and 6-OHDA-Induced Parkinson’s Disease Models
Hyun Joo Ham1,†, In Jun Yeo1,†, Seong Hee Jeon1, Jun Hyung Lim1, Sung Sik Yoo1, Dong Ju Son1, Sung-Su Jang2, Haksup Lee2, Seung-Jin Shin2, Sang Bae Han1, Jae Suk Yun1 and Jin Tae Hong1,*
1College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju 28644,
2ATGC Co., Seoul 06372, Republic of Korea
Tel: +82-43-261-2813, Fax: +82-43-268-2732
The first two authors contributed equally to this work.
Received: April 20, 2021; Revised: May 13, 2021; Accepted: May 17, 2021; Published online: June 3, 2021.
© The Korean Society of Applied Pharmacology. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Recently, increasing evidence suggests that neuroinflammation may be a critical factor in the development of Parkinson’s disease (PD) in addition to the ratio of acetylcholine/dopamine because dopaminergic neurons are particularly vulnerable to inflammatory attack. In this study, we investigated whether botulinum neurotoxin A (BoNT-A) was effective for the treatment of PD through its anti-neuroinflammatory effects and the modulation of acetylcholine and dopamine release. We found that BoNT-A ameliorated MPTP and 6-OHDA-induced PD progression, reduced acetylcholine release, levels of IL-1β, IL-6 and TNF-α as well as GFAP expression, but enhanced dopamine release and tyrosine hydroxylase expression. These results indicated that BoNT-A had beneficial effects on MPTP or 6-OHDA-induced PD-like behavior impairments via its anti-neuroinflammation properties, recovering dopamine, and reducing acetylcholine release.
Keywords: Parkinson’s disease, Botulinum toxin A, Anti-neuroinflammation

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