Dihydroartemisinin alleviates oxidative stress in bleomycin-induced pulmonary fibrosis.

Life Sciences
Dong-Xia YangWen-Dan Yuan

Abstract

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. 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. 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). Our results indicated that dihydroartemisinin might decrease oxidative damage to attenuate lung injury and fibrosis.

Citations

Apr 17, 2020·Frontiers in Pharmacology·Ming XiaHong Liu
Dec 5, 2018·Journal of Cellular Physiology·Yang HeRenping Huang
Feb 7, 2021·BioFactors·Seyede Atefe HosseiniAmirhossein Sahebkar
Feb 2, 2020·Respiratory Physiology & Neurobiology·Kai WangLiwei Wang
Mar 11, 2021·Drug Design, Development and Therapy·Xiaoyuan WangRenping Huang
Jun 3, 2021·Pharmaceutics·Lívia A TavaresRicardo L C de Albuquerque-Júnior
Jul 16, 2021·American Journal of Respiratory Cell and Molecular Biology·Taishu TakeuchiKiyotaka Hitomi

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