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肺痹方通过调控BRP39/IL-17和TGF1/Smad3信号通路减轻博来霉素诱导的小鼠肺纤维化

Feibi Recipe Reduced Pulmonary Fibrosis Induced by Bleomycin in Mice by Regulating BRP39/IL-17 and TGF1/Smad3 Signal Pathways.

作者信息

Wang Wei, Liu Zhaoheng, Niu Jie, Yang Haojie, Long Qi, Liu Haoge, Gu Xiaofeng, Jiao Yang

机构信息

Respiratory Department, Chongqing Traditional Chinese Medicine Hospital, No. 6 Pan Xi Qi Zhi, Jiangbei District, Chongqing 400021, China.

School of Life Sciences, Beijing University of Chinese Medicine, Northeast Corner of the Intersection of Yang Guang Nan Da Jie and Bai Yang Dong Lu, Fangshan District, Beijing 102488, China.

出版信息

Evid Based Complement Alternat Med. 2020 Oct 12;2020:5814658. doi: 10.1155/2020/5814658. eCollection 2020.

Abstract

Fibrotic remodeling has become the result of many lung diseases, and these disorders can be categorized with known as well as unknown etiologies. Idiopathic pulmonary fibrosis is the most fatal disease among the unknown etiology. TGF1/Smad3 signal pathway plays an important role in lung fibrosis and epithelial regeneration. This study investigated the effects and mechanism of Feibi Recipe (FBR) on pulmonary fibrosis. In this experiment, C57BL/6 mice were used and bleomycin was used to induce the lung injury. Meanwhile, the study showed a significant reduction in pathological response and mediators of inflammation and fibrosis such as IL-6, ICAM-1, IL-13, IL-17, BRP-39, TGF1, Smad3, and Smad7 were identified. Collectively, the FBR appears to attenuate the lung injury and the modeling of fibrosis in mice.

摘要

纤维化重塑已成为许多肺部疾病的结果,这些疾病可根据已知和未知病因进行分类。特发性肺纤维化是病因不明的疾病中最致命的一种。转化生长因子1/ Smad3信号通路在肺纤维化和上皮再生中起重要作用。本研究探讨了肺痹方(FBR)对肺纤维化的影响及机制。在本实验中,使用C57BL/6小鼠,并用博来霉素诱导肺损伤。同时,研究显示病理反应以及炎症和纤维化介质如IL-6、ICAM-1、IL-13、IL-17、BRP-39、转化生长因子1、Smad3和Smad7显著减少。总体而言,肺痹方似乎可减轻小鼠的肺损伤和纤维化模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c557/7576352/890b44c5b804/ECAM2020-5814658.001.jpg

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