Abstract
Acetaminophen is a common analgesic and antipyretic compound which, when administered in high doses, has been associated with significant morbidity and mortality, secondary to hepatic toxicity. Although this may be due to a direct interaction of reactive acetaminophen metabolites with hepatocyte proteins, recent studies have suggested that reactive species produced by neutrophils also contribute to the pathophysiological process. Researches on the chemical composition of B. trimera show that this plant has bioactive compounds such as flavonoids, related to the organism’s protection against free radicals. Therefore, in the present study, using Fischer rats, the effect of B. trimera on the antioxidant defense system, the production of nitric oxide (NO) and on the expression of nitric oxide synthase (iNOS), superoxide dismutase (SOD), catalase (CAT) and of the subunits of the NADPH oxidase in neutrophils was evaluated in a model of phagocytosis induced by zimosan (ZC3b) and in a model of inflammation induced by acetaminophen. The results show that the treatment with B. trimera improves the defense system of antioxidant and restores the balance ROS / NO that is altered in the inflammatory process induced by APAP. In conclusion, B. trimera extracts exert antioxidant properties by scavenging ROS and decrease the expression of genes responsible by reactive species production in neutrophils.
Keywords: Acetaminophen, Antioxidant enzymes, Baccharis trimera, NADPH oxidase, Neutrophils, qRT-PCR.
Current Pharmaceutical Biotechnology
Title:Baccharis trimera Improves the Antioxidant Defense System and Inhibits iNOS and NADPH Oxidase Expression in a Rat Model of Inflammation
Volume: 14 Issue: 11
Author(s): Bruno da Cruz Padua, Joamyr Victor Rossoni Junior, Cíntia Lopes de Brito Magalhaes, Janaina Brandao Seiberf, Carolina Morais Araujo, Gustavo Henrique Bianco de Souza, Miriam Martins Chaves, Marcelo Eustaquio Silva, Maria Lucia Pedrosa and Daniela Caldeira Costa
Affiliation:
Keywords: Acetaminophen, Antioxidant enzymes, Baccharis trimera, NADPH oxidase, Neutrophils, qRT-PCR.
Abstract: Acetaminophen is a common analgesic and antipyretic compound which, when administered in high doses, has been associated with significant morbidity and mortality, secondary to hepatic toxicity. Although this may be due to a direct interaction of reactive acetaminophen metabolites with hepatocyte proteins, recent studies have suggested that reactive species produced by neutrophils also contribute to the pathophysiological process. Researches on the chemical composition of B. trimera show that this plant has bioactive compounds such as flavonoids, related to the organism’s protection against free radicals. Therefore, in the present study, using Fischer rats, the effect of B. trimera on the antioxidant defense system, the production of nitric oxide (NO) and on the expression of nitric oxide synthase (iNOS), superoxide dismutase (SOD), catalase (CAT) and of the subunits of the NADPH oxidase in neutrophils was evaluated in a model of phagocytosis induced by zimosan (ZC3b) and in a model of inflammation induced by acetaminophen. The results show that the treatment with B. trimera improves the defense system of antioxidant and restores the balance ROS / NO that is altered in the inflammatory process induced by APAP. In conclusion, B. trimera extracts exert antioxidant properties by scavenging ROS and decrease the expression of genes responsible by reactive species production in neutrophils.
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Cruz Padua da Bruno, Rossoni Junior Victor Joamyr, de Brito Magalhaes Lopes Cíntia, Seiberf Brandao Janaina, Araujo Morais Carolina, Bianco de Souza Henrique Gustavo, Chaves Martins Miriam, Silva Eustaquio Marcelo, Pedrosa Lucia Maria and Costa Caldeira Daniela, Baccharis trimera Improves the Antioxidant Defense System and Inhibits iNOS and NADPH Oxidase Expression in a Rat Model of Inflammation, Current Pharmaceutical Biotechnology 2013; 14 (11) . https://dx.doi.org/10.2174/1389201014666131226151728
DOI https://dx.doi.org/10.2174/1389201014666131226151728 |
Print ISSN 1389-2010 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4316 |
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