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麻杏石甘汤通过抑制上皮-间质转化（EMT）和上皮屏障破坏来预防PM2.5诱导的肺损伤。

Ma Xing Shi Gan Decoction Protects against PM2.5-Induced Lung Injury through Suppression of Epithelial-to-Mesenchymal Transition (EMT) and Epithelial Barrier Disruption.

作者信息

Wang Ye-Fang, Fei Yu-Xiang, Zhao Bo, Yin Qi-Yang, Zhu Jian-Ping, Ren Guang-Hui, Wang Bo-Wen, Fang Wei-Rong, Li Yun-Man

机构信息

Department of Paediatrics, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Nanjing 210014, China.

State Key Laboratory of Natural Medicines, School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

出版信息

Evid Based Complement Alternat Med. 2020 Jun 17;2020:7176589. doi: 10.1155/2020/7176589. eCollection 2020.

DOI:10.1155/2020/7176589
PMID:32655666
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7317335/
Abstract

This research was designed to explore the effect of Ma Xing Shi Gan decoction (MXD) in alleviating particulate matter less than 2.5 m in diameter (PM2.5) induced lung injury from the perspective of epithelial barrier protection and inhibition of epithelial-to-mesenchymal transition (EMT). Rats were exposed to PM2.5 to establish a lung injury model in vivo, and a PM2.5-stimulated primary cultured type II alveolar epithelial cell model was introduced in vitro. Our results indicated that MXD alleviated the weight loss and pathologic changes and improved the epithelial barrier dysfunction. MXD also significantly inhibited the TGF-/Smad3 pathway, increased the level of ZO-1 and claudin-5, and reversed the EMT process. Notably, the protection of MXD was abolished by TGF- in vitro. Our results indicated that MXD has a protection against PM2.5-induced lung injury. The proposed mechanism is reversing PM2.5-induced EMT through inhibiting TGF-/Smad3 pathway and then upregulating the expression of tight-junction proteins.

摘要

本研究旨在从上皮屏障保护和抑制上皮-间质转化（EMT）的角度，探讨麻杏石甘汤（MXD）在减轻直径小于2.5微米的颗粒物（PM2.5）诱导的肺损伤中的作用。在体内将大鼠暴露于PM2.5以建立肺损伤模型，并在体外引入PM2.5刺激的原代培养II型肺泡上皮细胞模型。我们的结果表明，MXD减轻了体重减轻和病理变化，并改善了上皮屏障功能障碍。MXD还显著抑制TGF-/Smad3信号通路，增加ZO-1和claudin-5的水平，并逆转EMT过程。值得注意的是，在体外TGF-消除了MXD的保护作用。我们的结果表明，MXD对PM2.5诱导的肺损伤具有保护作用。其机制是通过抑制TGF-/Smad3信号通路，进而上调紧密连接蛋白的表达，逆转PM2.5诱导的EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b4/7317335/cbfece03cc94/ECAM2020-7176589.009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b4/7317335/7359e025f724/ECAM2020-7176589.005.jpg
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