BMB Reports 2018; 51(11): 590-595  https://doi.org/10.5483/BMBRep.2018.51.11.123
3-(Naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride attenuates MPP-induced cytotoxicity by regulating oxidative stress and mitochondrial dysfunction in SH-SY5Y cells
Seung-Ju Yang1,#, Ji Woong Yang2,#, Jung-Min Na2, Ji Sun Ha1, Soo Young Choi3 & Sung-Woo Cho2,*
1Department of Biomedical Laboratory Science, Konyang University, Daejeon 35365, 2Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, 3Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chunchon 24252, Korea
Correspondence to: Tel: +82-2-3010-4278; Fax: +82-2-3010-4278; E-mail: swcho@amc.seoul.kr
#These authors contributed equally to this work.
Received: June 4, 2018; Revised: June 20, 2018; Accepted: June 28, 2018; Published online: November 30, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Parkinson's disease (PD) is a common chronic neurodegenerative disease mainly caused by the death of dopaminergic neurons. However, no complete pharmacotherapeutic approaches are currently available for PD therapies. 1-methyl-4-phenylpyridinium (MPP)-induced SH-SY5Y neurotoxicity has been broadly utilized to create cellular models and study the mechanisms and critical aspects of PD. In the present study, we examined the role of a novel azetidine derivative, 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride (KHG26792), against MPP-induced neurotoxicity in SH-SY5Y cells. Treatment of KHG26792 significantly attenuated MPP-induced changes in the protein levels of Bcl-2 and Bax together with efficient suppression of MPP-induced activation of caspase-3 activity. KHG26792 also attenuated mitochondrial potential and levels of ROS, Ca2, and ATP in MPP-treated SH-SY5Y cells. Additionally, KHG26792 inhibited the induced production of nitric oxide and malondialdehyde. Moreover, the protective effect of KHG26792 is mediated through regulation of glutathione peroxidase and GDNF levels. Our results suggest a possibility that KHG26792 treatment significantly protects against MPP-induced neurotoxicity in SH-SY5Y cells and KHG26792 may be a valuable therapeutic agent for the treatment of PD induced by an environmental toxin.
Keywords: Azetidine derivative, Mitochondrial dysfunctions, MPP, Oxidative stress


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