Effects of Nervilia fordii Extract on Pulmonary Fibrosis Through TGF-β/Smad Signaling Pathway

• DOI: 10.3389/fphar.2021.659627
• Publication Date: 2021-04-19T08:23:56Z
• Authors: Yufeng Yao; Yue Yuan; Zenghui Lu; Yunxia Ma; Yuanyuan Xie; Meiqi Wang; Fangle Liu; Chenchen Zhu; Chaozhan Lin
• Keywords: Pharmacology; 0301 basic medicine; 03 medical and health sciences; pulmonary fibrosis; effective substances and mechanism; Nervilia fordii; Therapeutics. Pharmacology; RM1-950; TGF-β/Smad signaling pathway; Network pharmacology analysis; 3. Good health

Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial disease with poor prognosis. The extract of Nervilia fordii (NFE) has shown remarkable benefit in the treatment acute lung injury, cancer, severe respiratory syndrome (SARS). However, potential mechanism efficacy NFE IPF remain unknown. In this study, systematic network pharmacology analysis was used to predict IPF, based on major components elucidated by UPLC-TOF-MS/MS. molecular interactions between compounds targets were predicted using docking. vivo , rats induced single intratracheal injection bleomycin (BLM) orally administered for 14 days. Lung index biochemical levels determined, histopathological hematoxylin eosin (H&E) Masson staining performed. effects fibroblast proliferation Lipopolysaccharide (LPS) TGF-β1-induced mouse 3T6 fibroblasts evaluated vitro . total, 20 identified NFE, 102 predicted. These potentially participate processes regulated transmembrane receptor protein tyrosine kinase, ERBB2, et al. Molecular docking results high affinity three (rhamnazin, rhamnetin, rhamnocitrin) targets, suggesting that TGF-β most important target fibrosis. significantly decreased alleviated BLM-induced rats. Histopathological observation tissues showed inflammation collagen deposition inhibited migration LPS- fibroblasts, reduced contents hydroxyproline collagen, contributed anti-inflammation anti-oxidation. With intervention RNA expression TGF-β1, -SMA, Smad3/4, p -Smad3/4, CTGF, -ERK1/2 downregulated, while Smad7 ERK1/2 upregulated findings indicated may exert therapeutic alleviating inflammation, oxidation, deposition. related inhibition TGF-β/Smad signaling pathway.