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Ellagic acid ameliorates lung damage in rats via modulating antioxidant activities, inhibitory effects on inflammatory mediators and apoptosis-inducing activities.
Aslan, Abdullah; Hussein, Yousif Taha; Gok, Ozlem; Beyaz, Seda; Erman, Orhan; Baspinar, Serpil.
Afiliação
  • Aslan A; Faculty of Science, Department of Biology-Molecular Biology and Genetics Program, Firat University, Elazig, Turkey. aaslan@firat.edu.tr.
  • Hussein YT; Faculty of Science, Department of Biology, Firat University, Elazig, Turkey.
  • Gok O; Nursing Department, Halabja Technical Institute, Sulaimani Polytechnic University, Sulaimani, Iraq.
  • Beyaz S; Faculty of Science, Department of Biology, Firat University, Elazig, Turkey.
  • Erman O; Faculty of Science, Department of Biology, Firat University, Elazig, Turkey.
  • Baspinar S; Faculty of Science, Department of Biology, Firat University, Elazig, Turkey.
Environ Sci Pollut Res Int ; 27(7): 7526-7537, 2020 Mar.
Article em En | MEDLINE | ID: mdl-31885062
ABSTRACT
Phytochemicals is considered one of the most effective and safe alternative therapy against oxidative linked lung diseases. Ellagic acid (EA), an important component of fruits, nuts, and vegetables, are partly responsible for their beneficial health effects against oxidation-related diseases. In the present study, we investigated the ameliorative effect of EA on lung damage induced by carbon tetrachloride (CCl4) in Wistar male albino rats. Thirty-six male rats (n = 36, 8-week old) were divided into 4 groups, each with 9 rats. The groups were Control group received standard diet; EA group administered with EA (10 mg/kg body weight, intraperitoneal); CCl4 group administered with CCl4 (1.5 mg/kg body weight, intraperitoneal); EA+CCl4 group administered with EA and CCl4. . The rats were decapitated at the end of experimental period of 8 weeks and the lung tissues were examined. CCl4-induced rats showed elevation in the expressions of inflammatory proteins, nuclear factor kappa b (NF-κB), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α); and the indicator of lipid peroxidation, malondialdehyde (MDA). Intraperitoneal administration of EA significantly reduced the levels of these markers. EA administration increased the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf-2) and enhanced the activity of glutathione (GSH) and catalase enzyme (CAT). In addition, EA administration increased the expression levels of the executioner protein of apoptosis, caspase-3, and decreasing pro-survival protein, B cell lymphoma-2 (Bcl-2). In conclusion, these results establishes the protective role of EA in the treatment of lung damage and that in the future, this may have the potential to be used as a medication for the prevention or attenuation of lung diseases. Graphical abstract.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Ácido Elágico / Pulmão / Antioxidantes Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Ácido Elágico / Pulmão / Antioxidantes Idioma: En Ano de publicação: 2020 Tipo de documento: Article