大黄素
矽肺
上皮-间质转换
炎症
细胞凋亡
肺纤维化
纤维化
波形蛋白
体内
化学
药理学
癌症研究
医学
免疫学
A549电池
病理
生物
下调和上调
生物化学
生物技术
免疫组织化学
基因
作者
Xinru Pang,Linlin Shao,Xiangmin Nie,Haiyue Yan,Chao Li,Abrey J. Yeo,Martin F. Lavin,Qing Xia,Hua Shao,Gongchang Yu,Qiang Jia,Cheng Peng
标识
DOI:10.1016/j.intimp.2020.107277
摘要
Silicosis is a fatal pulmonary disease caused by the inhalation of silica dust, and characterized by inflammation and fibrosis of the lung, with no effective treatment to date. Here we investigate the effect of emodin, an anthraquinone derivative isolated from rhubarb using a mouse silicosis model and in vitro cultured human macrophages and alveolar epithelial cells. Results from histological examination indicated that emodin reduced the degree of alveolitis and fibrosis in the lungs of mice exposed to silica particles. We also demonstrated that emodin effectively inhibited the phosphorylation of Smad3 and NF-κB and reduced the levels of inflammatory factors in the lung tissue of mice treated with silica particles. In addition, we found that emodin inhibited apoptosis and demonstrated an anti-fibrotic effect by down-regulating the pro-apoptotic protein Bax and up-regulating the anti-apoptotic protein Bcl-2. Furthermore, emodin increased E-cadherin levels, reduced the expression of Vimentin, α-SMA and Col-I, as well as pro-inflammatory factors TGF-β1, TNF-α and IL-1β in vivo and in vitro. These results suggested that emodin can regulate epithelial–mesenchymal transition (EMT) through the inhibition of the TGF-β1/Smad3 signaling pathway and the NF-κB signaling pathway to prevent alveolar inflammation and apoptotic process. Overall, this study showed that emodin can alleviate pulmonary fibrosis in silicosis through regulating the inflammatory response and fibrotic process at multiple levels.
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