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Title: Baccharis trimera improves the antioxidant defense system and inhibits iNOS and NADPH oxidase expression in a rat model of inflammation.
Authors: Pádua, Bruno da Cruz
Rossoni Júnior, Joamyr Victor
Magalhães, Cíntia Lopes de Brito
Seibert, Janaína Brandão
Araújo, Carolina Morais
Souza, Gustavo Henrique Bianco de
Chaves, Míriam Martins
Silva, Marcelo Eustáquio
Pedrosa, Maria Lúcia
Costa, Daniela Caldeira
Keywords: Acetaminophen
Antioxidant enzymes
Issue Date: 2013
Citation: PÁDUA, B. da C. et al. Baccharis trimera improves the antioxidant defense system and inhibits iNOS and NADPH oxidase expression in a rat model of inflammation. Current Pharmaceutical Biotechnology, v. 14, p. 975-984, 2014. Disponível em: <>. Acesso em: 23 fev. 2017.
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.
ISSN: 1873-4316
Appears in Collections:DECBI - Artigos publicados em periódicos

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