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Abstract Title:

Ellagic acid ameliorates lung damage in rats via modulating antioxidant activities, inhibitory effects on inflammatory mediators and apoptosis-inducing activities.

Abstract Source:

Environ Sci Pollut Res Int. 2019 Dec 29. Epub 2019 Dec 29. PMID: 31885062

Abstract Author(s):

Abdullah Aslan, Yousif Taha Hussein, Ozlem Gok, Seda Beyaz, Orhan Erman, Serpil Baspinar

Article Affiliation:

Abdullah Aslan

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 (CCl) 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); CClgroup: administered with CCl(1.5 mg/kg body weight, intraperitoneal); EA+CClgroup: administered with EA and CCl. . The rats were decapitated at the end of experimental period of 8 weeks and the lung tissues were examined. CCl-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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