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Botulinum Toxin A Ameliorates Neuroinflammation in the MPTP and 6-OHDA-Induced Parkinson's Disease Models

  • Ham, Hyeon Joo (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Yeo, In Jun (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Jeon, Seong Hee (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Lim, Jun Hyung (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Yoo, Sung Sik (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Son, Dong Ju (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Jang, Sung-Su (ATGC Co.) ;
  • Lee, Haksup (ATGC Co.) ;
  • Shin, Seung-Jin (ATGC Co.) ;
  • Han, Sang Bae (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Yun, Jae Suk (College of Pharmacy and Medical Research Center, Chungbuk National University) ;
  • Hong, Jin Tae (College of Pharmacy and Medical Research Center, Chungbuk National University)
  • Received : 2021.04.20
  • Accepted : 2021.05.17
  • Published : 2022.01.01

Abstract

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

Acknowledgement

This work is financially supported by the National Research Foundation of Korea [NRF] Grant funded by the Korea government (MSIP) (No. MRC, 2017R1A5A2015541).

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