Intervention effect of dihydroartemisinin on pulmonary fibrosis in rats

Abstract

Objective To investigate the effect of dihydroartemisinin on pulmonary fibrosis and its mechanism in rats. Methods Seventy-five SD rats were randomly divided into 5 groups: the control group, the model group, the high dihydroartemisinin group, the low dihydroartemisinin group, and the prednisone group(15 rats in each group). Saline(9 g/L, 0.3 mL )was injected into the rat trachea of the control group, and the rats of the rest 4 groups were injected bleomycin(3 mg/kg). The rats in the control group and the model group received saline lavage ( 9 g/L, 3 mL), while the rats in the high dihydroartemi-sinin group and the low dihydroartemisinin group received dihydroartemisinin lavage (100, 50 mg/kg), and the rats in the prednisone group received prednisone lavage each day. Five rats in each group were sacrificed and lung tissues were removed on the 8th, 15th, and 29th day of lavage, and the degree of inflammation in lung tissue was observed by HE staining. The deposit of collagen in lung tissue was observed by Masson staining. The expressions of transforming growth factor β1(TGF-β1), collagen Ⅰand collagen Ⅲ in pneumonic tissues were detected by immunohistochemistry. Results The degree of inflammation in pneumonic tissues in the high dihydroartemisinin group, the low dihydroartemisinin group, and the prednisone group were less significantly than that in the model group(all P 0.05). TGF-β1, collagen Ⅰand collagen Ⅲ in lung tissues in the high dihydroartemisinin group and the prednisone group were lower than those in the model group(P 0.05), except that collagen Ⅲ expression in lung tissues was lower than that of the prednisone group on the 29th day(P>0.05). Conclusions Dihydroartemisinin can lessen the extent of pulmonary fibrosis in rats and its anti-fibrosis effect is dose-dependent. The anti-fibrosis effect of dihydroartemisinin may decrease the deposit of collagens in the lung tissues by inhibiting TGF-β1 expression in the lung tissues and have an effect of antifibrosis. Key words: Dihydroartemisinin; Pulmonary fibrosis; Transforming growth factor β1; Collagen Ⅰ; Collagen Ⅲ