Protective effects of propolis extract against nicotine-evoked pulmonary and hepatic damage.

Abstract

There is increasing interest in the use of natural products to treat many diseases, considering the minimal toxicity, availability, and low cost. Propolis, a natural resinous product produced by honeybees, has been proven for its antioxidant and anti-inflammatory properties. Therefore, this study was designed to investigate the protective potential of propolis extract against nicotine-induced pulmonary and hepatic damage in rats. Sprague Dawley rats were divided into six groups: control, propolis (200 and 300 mg/kg, p.o.), nicotine (10 mg/kg, i.p), and nicotine plus propolis-treated groups. Nicotine and propolis were given every day for 8 weeks. Then, blood and bronchoalveolar lavage fluid (BALF) were collected for assessing liver and lung functions. Liver and lung tissues were also harvested to assess oxidative stress and inflammatory biomarkers in addition to histopathological and immunohistochemical analysis. Both doses of propolis significantly decreased AST, ALT, ALP, and total and differential cell counts in a dose-dependent manner. Propolis extract significantly attenuated oxidative stress in both lung and liver tissues. The restoration of antioxidant status (GSH level, SOD activities) and reduction of nitric oxide and MDA content was more so in propolis 300-treated than propolis 200-treated group. This was parallel to the improvement seen in histopathological examination. Propolis 200 and 300 significantly decreased Nrf2 expression and increased HO-1 expression in a dose-dependent manner. Moreover, immunohistochemical examination revealed that propolis 200 and 300 decreased the expression of iNOS in lung and liver tissues while decreased TNF-α expression in lung tissues only. Propolis extract could have a protective potential against nicotine-induced pulmonary and hepatic damage via activating Nrf2/HO-1 signaling.