Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity
ABSTRACT Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edarav...
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doaj-edb5ae4ffdb8416db10dc991ea4f8a4a2020-11-24T23:53:32ZengInstituto de Tecnologia do Paraná (Tecpar)Brazilian Archives of Biology and Technology1678-432459010.1590/1678-4324-2016160093S1516-89132016000100342Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicityMotahareh KoohsariFatemeh ShakiDaniel JahaniABSTRACT Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METH-induced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132016000100342&lng=en&tlng=enEdaravoneMethamphetaminecardiotoxicityOxidative stressMitochondria |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Motahareh Koohsari Fatemeh Shaki Daniel Jahani |
spellingShingle |
Motahareh Koohsari Fatemeh Shaki Daniel Jahani Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity Brazilian Archives of Biology and Technology Edaravone Methamphetamine cardiotoxicity Oxidative stress Mitochondria |
author_facet |
Motahareh Koohsari Fatemeh Shaki Daniel Jahani |
author_sort |
Motahareh Koohsari |
title |
Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity |
title_short |
Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity |
title_full |
Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity |
title_fullStr |
Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity |
title_full_unstemmed |
Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity |
title_sort |
protective effects of edaravone against methamphetamine-induced cardiotoxicity |
publisher |
Instituto de Tecnologia do Paraná (Tecpar) |
series |
Brazilian Archives of Biology and Technology |
issn |
1678-4324 |
description |
ABSTRACT Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METH-induced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease. |
topic |
Edaravone Methamphetamine cardiotoxicity Oxidative stress Mitochondria |
url |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132016000100342&lng=en&tlng=en |
work_keys_str_mv |
AT motaharehkoohsari protectiveeffectsofedaravoneagainstmethamphetamineinducedcardiotoxicity AT fatemehshaki protectiveeffectsofedaravoneagainstmethamphetamineinducedcardiotoxicity AT danieljahani protectiveeffectsofedaravoneagainstmethamphetamineinducedcardiotoxicity |
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