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Subject Area

Obstetrics and Gynecology

Article Type

Review

Abstract

Objective This work aims to investigate the effect of atorvastatin on bleomycin-induced pulmonary fibrosis in rats. Background Pulmonary fibrosis is a lung disease refractory to treatment with poor prognosis. It is characterized by progressive irreversible destruction of lung architecture resulting from scar formation and organ dysfunction. Atorvastatin ameliorates pulmonary fibrosis in rats via having antioxidant and antifibrotic effects. Materials and methods The study was conducted for 3 weeks using 30 male Wister albino rats divided into three groups of 10 rats each as follows. Group 1: injected with saline intratracheal single dose and received saline orally. Group 2: injected with a single intratracheal dose of bleomycin (1 mg/kg) and received saline orally. Group 3: injected with bleomycin intratracheal and received atorvastatin (10 mg/kg/day) orally. The following procedures were done: (a) baseline body weight, final body weight, lung weight, and lung coefficient. (b) Biochemical measurements: lung malondialdehyde (MDA), lung reduced glutathione (GSH), and serum transforming growth factor-β1 (TGF-β1). (c) Histopathological examination of hematoxylin and eosin and Masson's trichrome stained sections followed by α-smooth muscle actin (α-SMA) immunostaining. Results Toxic group (group 2) showed a significant decrease in body weight and lung GSH associated with increase in lung weight, lung coefficient, serum TGF-β1, lung MDA level, histopathological fibrosis score, and H-sore of α-SMA compared with the normal group (group 1). In contrast, atorvastatin-treated group (group 3) showed a significant increase in body weight and lung GSH with reduction in lung weight, lung coefficient, serum TGF-β1, lung MDA level, histopathological fibrosis score, and H-sore of α-SMA compared with (group 2), but still significant to normal group levels. Conclusion It is concluded that atorvastatin attenuated bleomycin-induced pulmonary fibrosis in rats by reduction of oxidative stress markers, suppression of TGF-β1, and improving fibrosis score and H-score of α-SMA.

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