Aims: Dihydroartemisinin has been shown to inhibit the development of pulmonary fibrosis in rats, but its mechanism has yet to be elucidated. This study aimed to determine the mechanisms of dihydroartemisinin in bleomycin-induced pulmonary fibrosis in a rat model.
Main methods: Morphological changes and collagen deposition were analyzed via hematoxylin-eosin staining and Masson staining and the expression of biotic-factor-related oxidative stress in lung tissues was assayed with standard assay kits. The expressions of α-SMA, E-cadherin, and Nrf2/HO-1 were detected by Western blot and RT-PCR, and the cell morphology and proliferation of cultured type II alveolar epithelial cells (AECs) were assessed via microscopy and immunocytochemical assay.
Key findings: Dihydroartemisinin treatment significantly decreased the level of oxidative stress and collagen synthesis and inhibited AECs differentiation in bleomycin-induced pulmonary fibrosis compared to the control group (P < 0.001).
Significance: Our results indicated that dihydroartemisinin might decrease oxidative damage to attenuate lung injury and fibrosis.
Keywords: Bleomycin; Dihydroartemisinin; Oxidative stress; Pulmonary fibrosis.
Copyright © 2017. Published by Elsevier Inc.