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Melatonin Protects SH-SY5Y Neuronal Cells Against Methamphetamine-Induced Endoplasmic Reticulum Stress and Apoptotic Cell Death.
Neurotox Res. 2017 01; 31(1):1-10.NR

Abstract

Methamphetamine (METH), a psychostimulant with highly neurotoxic effects, has been known to induce neuronal apoptosis in part through an endoplasmic reticulum (ER) stress pathway. Melatonin is an endogenous antioxidant compound that exerts protective effects against several neurodegenerative conditions, including METH-induced neurotoxicity, via various mechanisms. However, the role of melatonin in ER stress is still relatively unclear. In the present study, we investigated ER stress and neuronal apoptosis following METH treatment and the role of melatonin in METH-mediated ER stress-induced cell death in the SH-SY5Y neuroblastoma cell line. We found that METH caused the overexpression of ER stress-related genes, including C/EBP homologous protein and spliced X-box binding protein 1, in dose- and time-dependent manners. Moreover, METH time-dependently activated caspase-12 and -3, leading to cellular apoptosis. Furthermore, we demonstrated that pretreatment with melatonin attenuated the overexpression of ER stress-related genes and the cleavages of caspase-12 and -3 caused by METH exposure. Flow cytometry revealed that METH-mediated neuronal apoptosis was also prevented by melatonin. These findings suggest the protective effects of melatonin against ER stress and apoptosis caused by METH and other harmful agents.

Authors+Show Affiliations

Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakornpathom, 73170, Thailand. piyarat.gov@mahidol.ac.th.Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakornpathom, 73170, Thailand. Center for Neuroscience and Department of Pharmacology, Faculty of Science, Mahidol University, Rama VI Road, Bangkok, 10400, Thailand.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27370255

Citation

Wongprayoon, Pawaris, and Piyarat Govitrapong. "Melatonin Protects SH-SY5Y Neuronal Cells Against Methamphetamine-Induced Endoplasmic Reticulum Stress and Apoptotic Cell Death." Neurotoxicity Research, vol. 31, no. 1, 2017, pp. 1-10.
Wongprayoon P, Govitrapong P. Melatonin Protects SH-SY5Y Neuronal Cells Against Methamphetamine-Induced Endoplasmic Reticulum Stress and Apoptotic Cell Death. Neurotox Res. 2017;31(1):1-10.
Wongprayoon, P., & Govitrapong, P. (2017). Melatonin Protects SH-SY5Y Neuronal Cells Against Methamphetamine-Induced Endoplasmic Reticulum Stress and Apoptotic Cell Death. Neurotoxicity Research, 31(1), 1-10. https://doi.org/10.1007/s12640-016-9647-z
Wongprayoon P, Govitrapong P. Melatonin Protects SH-SY5Y Neuronal Cells Against Methamphetamine-Induced Endoplasmic Reticulum Stress and Apoptotic Cell Death. Neurotox Res. 2017;31(1):1-10. PubMed PMID: 27370255.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Melatonin Protects SH-SY5Y Neuronal Cells Against Methamphetamine-Induced Endoplasmic Reticulum Stress and Apoptotic Cell Death. AU - Wongprayoon,Pawaris, AU - Govitrapong,Piyarat, Y1 - 2016/07/01/ PY - 2016/06/14/received PY - 2016/06/21/accepted PY - 2016/06/20/revised PY - 2016/7/3/pubmed PY - 2017/7/29/medline PY - 2016/7/3/entrez KW - Apoptosis KW - Endoplasmic reticulum stress KW - Melatonin KW - Methamphetamine SP - 1 EP - 10 JF - Neurotoxicity research JO - Neurotox Res VL - 31 IS - 1 N2 - Methamphetamine (METH), a psychostimulant with highly neurotoxic effects, has been known to induce neuronal apoptosis in part through an endoplasmic reticulum (ER) stress pathway. Melatonin is an endogenous antioxidant compound that exerts protective effects against several neurodegenerative conditions, including METH-induced neurotoxicity, via various mechanisms. However, the role of melatonin in ER stress is still relatively unclear. In the present study, we investigated ER stress and neuronal apoptosis following METH treatment and the role of melatonin in METH-mediated ER stress-induced cell death in the SH-SY5Y neuroblastoma cell line. We found that METH caused the overexpression of ER stress-related genes, including C/EBP homologous protein and spliced X-box binding protein 1, in dose- and time-dependent manners. Moreover, METH time-dependently activated caspase-12 and -3, leading to cellular apoptosis. Furthermore, we demonstrated that pretreatment with melatonin attenuated the overexpression of ER stress-related genes and the cleavages of caspase-12 and -3 caused by METH exposure. Flow cytometry revealed that METH-mediated neuronal apoptosis was also prevented by melatonin. These findings suggest the protective effects of melatonin against ER stress and apoptosis caused by METH and other harmful agents. SN - 1476-3524 UR - https://www.unboundmedicine.com/medline/citation/27370255/Melatonin_Protects_SH_SY5Y_Neuronal_Cells_Against_Methamphetamine_Induced_Endoplasmic_Reticulum_Stress_and_Apoptotic_Cell_Death_ L2 - https://dx.doi.org/10.1007/s12640-016-9647-z DB - PRIME DP - Unbound Medicine ER -