活性氧
化学
卵清蛋白
转化生长因子
肺纤维化
上皮-间质转换
信号转导
下调和上调
癌症研究
氧化应激
免疫学
纤维化
细胞生物学
医学
生物
内科学
生物化学
基因
免疫系统
作者
Haizhu Zeng,Yumeng Wang,Yuxia Gu,Jinrui Wang,Huali Zhang,Hongchang Gao,Qinqin Jin,Lei Zhao
出处
期刊:Life Sciences
[Elsevier]
日期:2019-02-01
卷期号:218: 25-30
被引量:43
标识
DOI:10.1016/j.lfs.2018.08.013
摘要
Reactive oxygen species (ROS) and epithelial–mesenchymal transition (EMT) play a critical role in transforming growth factor (TGF)-β1-mediated fibrotic airway remodeling in asthma. Polydatin (PD) is a small natural molecule in Chinese medicine; it is isolated from Polygonum cuspidatum and has antioxidative properties. In this study, we aimed to determine whether PD was protective against ROS-induced pulmonary fibrosis in asthma. Ovalbumin (OVA) was used to induce asthma in a mouse model that was treated with or without PD. We also created nuclear factor erythroid 2-related factor 2 (Nrf2) knockdown BEAS-2B cells and investigated whether PD reversed TGF-β1-induced pulmonary epithelial cell EMT by promotion of Nrf2-mediated antioxidation. Immunofluorescence showed that ROS and TGF-β1 expression was significantly increased in lung tissue from the OVA-induced asthma model. PD treatment inhibited activity of ROS and TGF-β1. Immunohistochemistry showed that PD treatment decreased OVA-induced lung ROS, TGF-β1 expression and fibroblasts. Western blotting showed that PD treatment reversed OVA-induced NADPH oxidase (NOX)1/4 expression by promoting Nrf2-mediated heme oxygenase-1 and NADPH dehydrogenase (quinone)-1 expression. PD treatment suppressed OVA-induced EMT and lung fibroblast protein expression in lung tissue. Nrf2 downregulation suppressed the protective effect of PD by promoting TGF-β1-induced ROS and EMT and accumulation of extracellular-matrix-related protein. All these data indicate that PD has potential therapeutic effects in asthma by promoting Nrf2-mediated antioxidation.
科研通智能强力驱动
Strongly Powered by AbleSci AI