Repository of Research and Investigative Information

Repository of Research and Investigative Information

Ilam University of Medical Sciences

Neuroprotective Effects of the Small-Molecule Enhancer of Rapamycin in the Cellular Model of Parkinson's Disease

Mon Jun 27 09:39:12 2022

(2019) Neuroprotective Effects of the Small-Molecule Enhancer of Rapamycin in the Cellular Model of Parkinson's Disease. Neurophysiology. pp. 88-96. ISSN 0090-2977

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Abstract

Parkinson's disease (PD) is one of the most frequent neurodegenerative diseases. We investigated the protective effects of the small-molecule enhancer of rapamycin SMER28 in the SH-SY5Y cellular model of PD induced by 6-hydroxydopamine (6-OHDA). The cell viability and apoptosis estimations were performed using MTT and annexin V-FITC assays, respectively. The levels of intracellular reactive oxygen species (ROSs) and mitochondrial membrane potential were determined by the respective fluorescence detection. ELISA assays were performed to detect the levels of dopamine and alpha-synuclein. Additionally, mTOR signaling and the expression levels of autophagy-related proteins, including Beclin-1, p62, and LC3, were analyzed by Western blot. SMER28 increased the cell viability and mitochondrial membrane potential but decreased -synuclein and intracellular ROSs. SMER28 also reversed the decreased dopamine level and increased alpha-synuclein expression induced by 6-OHDA. The latter (100 mu M) induced intense apoptosis, but 50 mu M SMER28 prevented the latter via autophagy induction. We also noticed that SMER28 triggered autophagy and enhanced Beclin-1 expression, and LC3-I to LC3-II conversion, as well as decreased p62 expression and mTOR signaling activation in SH-SY5Y cells. Blocking of autophagy by a selective inhibitor, 3-methyladenosine, decreased the autophagy ratio in SMER28-treated SH-SY5Y cells, suggesting a considerable neuroprotective role of SMER28-induced autophagy. Taken together, it can be concluded that SMER28 exerts a protective effect against cellular damage induced by 6-OHDA via autophagy induction. Therefore, SMER28 may serve as a promising potential adjuvant therapy for PD treatment.

Item Type: Article
Creators:
CreatorsEmail
Darabi, S.UNSPECIFIED
Noori-Zadeh, A.UNSPECIFIED
Rajaei, F.UNSPECIFIED
Abbaszadeh, H. A.UNSPECIFIED
Abdollahifar, M. A.UNSPECIFIED
Bakhtiyari, S.UNSPECIFIED
Keywords: Parkinson's disease cellular model 6-OHDA apoptosis autophagy 3-methyladenosine dopaminergic neurons SH-SY5Y cells SMER28 dopaminergic-neurons stem-cell autophagy apoptosis damage dysfunction Neurosciences & Neurology Physiology
Divisions:
Page Range: pp. 88-96
Journal or Publication Title: Neurophysiology
Journal Index: ISI
Volume: 51
Number: 2
Identification Number: https://doi.org/10.1007/s11062-019-09798-5
ISSN: 0090-2977
Depositing User: مهندس مهدی شریفی
URI: http://eprints.medilam.ac.ir/id/eprint/2418

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