Dong-Xia Yang1, Jun Qiu2, Hui-Hui Zhou3, Yan Yu1, Dong-Li Zhou4, Yan Xu5, Ming-Zhe Zhu5, Xing-Ping Ge5, Jing-Min Li1, Chang-Jun Lv1, Hong-Qin Zhang6, Wen-Dan Yuan7. 1. College of Basic Medicine, Binzhou Medical University, Yantai, Shandong 264003, China. 2. Department of Blood Purification Center, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, China. 3. Department of pathology Center, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, China. 4. Shandong Laiyang Health School, Laiyang, Shandong 265200, China. 5. Pediatric Nephro Department, The Affiliated Hospital of Binzhou Medical University, Yantai, Shandong 264000, China. 6. College of Basic Medicine, Binzhou Medical University, Yantai, Shandong 264003, China. Electronic address: byzhhq@163.com. 7. College of Basic Medicine, Binzhou Medical University, Yantai, Shandong 264003, China. Electronic address: 981713509@qq.com.
Abstract
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.
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.
Authors: Lívia A Tavares; Allan A Rezende; Jymmys L Santos; Charles S Estevam; Ana M O Silva; Jaderson K Schneider; John L S Cunha; Daniela Droppa-Almeida; Ivan J Correia-Neto; Juliana C Cardoso; Patricia Severino; Eliana B Souto; Ricardo L C de Albuquerque-Júnior Journal: Pharmaceutics Date: 2021-05-09 Impact factor: 6.321