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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/34889
Title: Protective effect of melatonin on methamphetamine-induced apoptosis in glioma cell line
Authors: Pichaya Jumnongprakhon
Piyarat Govitrapong
Chainarong Tocharus
Wanida Tungkum
Jiraporn Tocharus
Chiang Mai University
Mahidol University
Naresuan University
Keywords: Neuroscience;Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Jan-2014
Citation: Neurotoxicity Research. Vol.25, No.3 (2014), 286-294
Abstract: Methamphetamine (METH) is a highly addictive drug causing neurodegenerative diseases. METH has been known to be neurotoxic by inducing oxidative stress, free radical, and pro-inflammatory cytokines. Previous studies have shown that METH could induce neuron and glial cell death, especially inducing glial cell-mediated neurotoxicity that plays a critical role in stress-induced central nervous system damage. Therefore, the aim of the present study is to explore the mechanisms of METH-induced cell death in the glial cell. METH-induced glial cells death is mediated via mitochondrial damage pathway. METH activates the upregulation of the Bax, cytochrome c, cleavage caspase 9 and 3 proteins, and downregulation of Bcl-XLprotein in cascade. Pretreatment with melatonin, a neurohormone secreted by the pineal gland, effectively reduced glial cell death. Moreover, melatonin increased the Bcl-XL/Bax ratio but reduced the level of cytochrome c, cleavage caspase 9 and 3 proteins. Therefore, these results demonstrated that melatonin could reduce the cytotoxic effect of METH by decreasing the mitochondrial death pathway activation in glial cells. This outcome suggests that melatonin might be beneficial as the neuroprotection in neurodegenerative diseases caused by METH or other pathogens. © 2013 Springer Science+Business Media.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84896030663&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/34889
ISSN: 14763524
10298428
Appears in Collections:Scopus 2011-2015

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