Kangfuxin Oral Liquid Attenuates Bleomycin-Induced Pulmonary Fibrosis via the TGF- β 1/Smad Pathway

Huan Yao; Shujun Wei; Yongjing Xiang; Ziqiang Wu; Weiwei Liu; Baojia Wang; Xueping Li; Huan Xu; Juan Zhao; Yongxiang Gao

doi:10.1155/2019/5124026

Kangfuxin Oral Liquid Attenuates Bleomycin-Induced Pulmonary Fibrosis via the TGF- β 1/Smad Pathway

Evid Based Complement Alternat Med. 2019 Nov 3:2019:5124026. doi: 10.1155/2019/5124026. eCollection 2019.

Authors

Huan Yao¹, Shujun Wei¹, Yongjing Xiang¹, Ziqiang Wu², Weiwei Liu¹, Baojia Wang¹, Xueping Li¹, Huan Xu^{1

2}, Juan Zhao³, Yongxiang Gao^{3

4}

Affiliations

¹ College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 11137, China.
² College Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 11137, China.
³ College of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 11137, China.
⁴ College of International Education, Chengdu University of Traditional Chinese Medicine, Chengdu 11137, China.

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal respiratory disease with a poor prognosis characterized by transforming growth factor (TGF)-β-induced proliferation, migration, and differentiation of fibroblasts, resulting in excessive extracellular matrix (ECM) deposition. Whether Kangfuxin oral liquid (KFXOL) has a protective function in pulmonary fibrosis is largely unknown. The goal of this study was to investigate the potential efficacy of KFXOL, as well as the underlying mechanism by which KFXOL regulates pulmonary fibrosis in vivo and in vitro. We found that KFXOL dramatically attenuated intratracheal bleomycin (BLM)-induced pulmonary fibrosis in terms of both severe alveolar architecture destruction and collagen deposition. KFXOL treatment significantly inhibited the proliferation, migration, and differentiation of pulmonary fibroblasts following activation using BLM/TGF-β1 and normalized the expression of ECM deposition-related proteins, including matrix metalloproteinase (MMP)-1, MMP-9, and tissue inhibitor of metalloproteinases 1. These effects were mediated via the inhibition of TGF-β1 and phosphorylated Smad2/3 activation in vivo. Taken together, our data suggest that KFXOL attenuates the development of pulmonary fibrosis via the TGF-β1/Smad signaling pathway and thus has potential utility in the treatment of pulmonary fibrosis.