دورية أكاديمية

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

التفاصيل البيبلوغرافية
العنوان: Mitochonic acid 5 ameliorates the motor deficits in the MPTP-induced mouse Parkinson’s disease model by AMPK-mediated autophagy
المؤلفون: Juan Wan, Yijiang Gao, Jian Tan, Shanqing Yi, Kailiang Huang, Yao Liu, Dong Chang, Jiali Xie, Shuangxi Chen, Heng Wu
المصدر: Folia Neuropathologica, Vol 60, Iss 3, Pp 329-337 (2022)
بيانات النشر: Termedia Publishing House, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine
مصطلحات موضوعية: parkinson’s disease (pd), mitochonic acid 5 (ma-5), ampk, autophagy., Medicine
الوصف: 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1641-4640
1509-572X
Relation: https://www.termedia.pl/Mitochonic-acid-5-ameliorates-the-motor-deficits-in-the-MPTP-induced-mouse-Parkinson-s-disease-model-by-AMPK-mediated-autophagy,20,47655,1,1.html; https://doaj.org/toc/1641-4640; https://doaj.org/toc/1509-572X
DOI: 10.5114/fn.2022.118796
URL الوصول: https://doaj.org/article/100057c4521145b48b001b246336bbdb
رقم الأكسشن: edsdoj.100057c4521145b48b001b246336bbdb
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16414640
1509572X
DOI:10.5114/fn.2022.118796