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...

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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
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Institution: Chiang Mai University
Language: English
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spelling th-cmuir.6653943832-41412014-08-30T02:35:43Z Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line Jumnongprakhon P. Govitrapong P. Tocharus C. Tungkum W. Tocharus J. 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. 2014-08-30T02:35:43Z 2014-08-30T02:35:43Z 2014 Article 14763524 10.1007/s12640-013-9419-y NURRF 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 English Springer New York LLC
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
language English
description 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.
format Article
author Jumnongprakhon P.
Govitrapong P.
Tocharus C.
Tungkum W.
Tocharus J.
spellingShingle Jumnongprakhon P.
Govitrapong P.
Tocharus C.
Tungkum W.
Tocharus J.
Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line
author_facet Jumnongprakhon P.
Govitrapong P.
Tocharus C.
Tungkum W.
Tocharus J.
author_sort Jumnongprakhon P.
title Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line
title_short Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line
title_full Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line
title_fullStr Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line
title_full_unstemmed Protective Effect of Melatonin on Methamphetamine-Induced Apoptosis in Glioma Cell Line
title_sort protective effect of melatonin on methamphetamine-induced apoptosis in glioma cell line
publisher Springer New York LLC
publishDate 2014
url 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
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