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Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats

Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzym...

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Autores principales: Pereira-Maróstica, Heloisa V., Castro, Lorena S., Gonçalves, Geferson A., Silva, Francielli M.S., Bracht, Lívia, Bersani-Amado, Ciomar A., Peralta, Rosane M., Comar, Jurandir F., Bracht, Adelar, Sá-Nakanishi, Anacharis B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826661/
https://www.ncbi.nlm.nih.gov/pubmed/31618993
http://dx.doi.org/10.3390/antiox8100485
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author Pereira-Maróstica, Heloisa V.
Castro, Lorena S.
Gonçalves, Geferson A.
Silva, Francielli M.S.
Bracht, Lívia
Bersani-Amado, Ciomar A.
Peralta, Rosane M.
Comar, Jurandir F.
Bracht, Adelar
Sá-Nakanishi, Anacharis B.
author_facet Pereira-Maróstica, Heloisa V.
Castro, Lorena S.
Gonçalves, Geferson A.
Silva, Francielli M.S.
Bracht, Lívia
Bersani-Amado, Ciomar A.
Peralta, Rosane M.
Comar, Jurandir F.
Bracht, Adelar
Sá-Nakanishi, Anacharis B.
author_sort Pereira-Maróstica, Heloisa V.
collection PubMed
description Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress.
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spelling pubmed-68266612019-11-18 Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats Pereira-Maróstica, Heloisa V. Castro, Lorena S. Gonçalves, Geferson A. Silva, Francielli M.S. Bracht, Lívia Bersani-Amado, Ciomar A. Peralta, Rosane M. Comar, Jurandir F. Bracht, Adelar Sá-Nakanishi, Anacharis B. Antioxidants (Basel) Article Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress. MDPI 2019-10-15 /pmc/articles/PMC6826661/ /pubmed/31618993 http://dx.doi.org/10.3390/antiox8100485 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Pereira-Maróstica, Heloisa V.
Castro, Lorena S.
Gonçalves, Geferson A.
Silva, Francielli M.S.
Bracht, Lívia
Bersani-Amado, Ciomar A.
Peralta, Rosane M.
Comar, Jurandir F.
Bracht, Adelar
Sá-Nakanishi, Anacharis B.
Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats
title Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats
title_full Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats
title_fullStr Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats
title_full_unstemmed Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats
title_short Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats
title_sort methyl jasmonate reduces inflammation and oxidative stress in the brain of arthritic rats
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826661/
https://www.ncbi.nlm.nih.gov/pubmed/31618993
http://dx.doi.org/10.3390/antiox8100485
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