eISSN: 1509-572x
ISSN: 1641-4640
Folia Neuropathologica
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vol. 60
Original paper

Mitochonic acid 5 ameliorates the motor deficits in the MPTP-induced mouse Parkinson’s disease model by AMPK-mediated autophagy

Juan Wan
1, 2
Yijiang Gao
1, 2
Jian Tan
1, 2
Shanqing Yi
1, 2
Kailiang Huang
Yao Liu
1, 2
Dong Chang
1, 2
Jiali Xie
1, 2
Shuangxi Chen
1, 2, 4
Heng Wu
1, 2

The First Affiliated Hospital, Department of Neurology, Multi-Omics Research Center for Brain Disorders, Hengyang Medical School, University of South China, Hengyang, Hunan, PR China
Clinical Research Center for Immune-Related Encephalopathy in Hunan Province, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, PR China
Department of Emergency, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, PR China
Health Center of Yumushan Town, Zhengxiang District, Hengyang, Hunan, PR China
Folia Neuropathol 2022; 60 (3): 329-337
Online publish date: 2022/10/11
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Parkinson’s disease (PD) is a well-known neurodegenerative disorder characterized by the degeneration of dopaminergic neurons, and oxidative stress and neuroinflammation are also associated with the pathogenesis of PD. Mitochonic acid 5 (MA-5), an analogue of indole-3-acetic acid, exerts key protective roles in inhibiting apoptosis, oxidative stress and neuroinflammation in multiple diseases. However, whether MA-5 can be beneficial for PD remains unclear. Hence, the aim of this study was to investigate the neuroprotective role of MA-5 in PD. In the current study, MPTP-challenged mice were treated as the in vivo model, and the effect of MA-5 on the motor function, neuronal survival, oxidative stress, neuroinflammation and the underlying mechanisms involved with AMPK and autophagy were determined. We revealed that MA-5 obviously up-regulated the phosphorylation of AMPK and promoted the autophagy (indicated by the increased LC3II/LC3I, parkin, pink and decreased p62) in substantia nigra (SN), ameliorated the motor deficits, up-regulated the expression of TH, suppressed the inflammation (indicated by the decreased protein levels of interleukin (IL)-1b, IL-6, tumour necrosis factor a) in SN in MPTP-induced mice. However, these patterns were reversed after the treatment of Compound C, an inhibitor of AMPK; also, after the application of CSA, an inhibitor of autophagy, MA-5 cannot play against the neurotoxicity of MPTP in mice. These combined results suggest that MA-5 can protect against MPTP-induced neurotoxicity to ameliorate the impaired motor function, which may be modulated via activation of AMPK-induced autophagy.

Parkinson’s disease (PD), mitochonic acid 5 (MA-5), AMPK, autophagy

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