Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line

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 g...

Full description

Saved in:
Bibliographic Details
Main Authors: Jumnongprakhon P., Govitrapong P., Tocharus C., Tungkum W., Tocharus J.
Format: Article
Language:English
Published: Springer New York LLC 2014
Online Access:http://www.scopus.com/inward/record.url?eid=2-s2.0-84896030663&partnerID=40&md5=7b8288d2c2b8054f89cff476d4eb6276
http://www.ncbi.nlm.nih.gov/pubmed/23975636
http://cmuir.cmu.ac.th/handle/6653943832/4141
Tags: Add Tag
No Tags, Be the first to tag this record!
Institution: Chiang Mai University
Language: English
Description
Summary: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-XL protein 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.