Preventive Effect of Chrysin on Bleomycin-Induced Lung Fibrosis in Rats
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The aim of the current study is determination of protective effect of chrysin (CRS), a natural flavonoid, on cell injury produced by lung fibrosis induced with bleomycin (BLC) in rats. Twenty-eight female rats were assigned to four groups as follows: control group, CRS group; 50 mg/kg CRS was continued orally for 14 days, BLC group; a single intratracheal injection of BLC (2.5 mg/kg body weight in 0.25 ml phosphate buffered saline), BLC + CRS group; 50 mg/kg CRS was administered 1 day before the intratracheal BLC injection and continued for 14 days orally. All animals were sacrificed at day 14th after BLC administration. The semiquantitative assessment of histopathological consisting of lung inflammation and collagen deposition, tissue levels of thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reducted glutathione (GSH) were measured. BLC provoked histological changes consisting of alveolar congestion, increase connective tissue, infiltration, and the thickness of alveolar wall were detected significantly when compared to the control group (p ≤ 0.0001). CRS supplementation significantly restored these histological damages (p ≤ 0.0001). The level of tissue TBARS was increased with BLC (p < 0.01). Increased level of TBARS was significantly reversed by CRS administration. Also, BLC administration reduced tissue activities of SOD, GPx, CAT, and GSH in the lung tissue compared to control group (p < 0.01). Furthermore, the reduction in activities of CAT, SOD, and level of GSH were prevented by CRS supplementation (p < 0.01). In this study, we demonstrated for the first time that CRS significantly prevents BLC-induced lung inflammation and fibrosis in rats. Further studies are needed to assess the role of CRS in the treatment of lung inflammation and fibrosis.
KEY WORDSantiinflammatory bleomycin chrysin pulmonary fibrosis idiopathic pulmonary fibrosis
Conflict of Interest
The authors have no conflict of interest to declare. This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
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