文献类型：期刊文献

英文题名：Qimai Feiluoping Decoction Inhibits EndMT to Alleviate Pulmonary Fibrosis by Reducing PI3K/ AKT/mTOR Pathway-Mediated the Restoration of Autophagy

作者：Ma, Jing[1];Ding, Lu[1];Zang, Xiaoyu[2];Yang, Yingying[3];Zhang, Wei[4];Li, Xiangyan[1];Zhao, Daqing[1];Zhang, Zepeng[1];Wang, Zeyu[1];Zhao, Linhua[1];Tong, Xiaolin[1]

第一作者：Ma, Jing

通信作者：Tong, XL[1]

机构：[1]Changchun Univ Tradit Chinese Med, Affiliated Hosp, Changchun 130021, Jilin, Peoples R China;[2]Changchun Univ Chinese Med, Coll Tradit Chinese Med, Changchun 130117, Jilin, Peoples R China;[3]China Japan Friendship Hosp, Natl Ctr Integrated Tradit Chinese & Western Med, Beijing 100029, Peoples R China;[4]Gansu Univ Chinese Med, Lanzhou 730000, Gansu, Peoples R China

第一机构：Changchun Univ Tradit Chinese Med, Affiliated Hosp, Changchun 130021, Jilin, Peoples R China

通信机构：[1]corresponding author), Changchun Univ Tradit Chinese Med, Affiliated Hosp, Changchun 130021, Jilin, Peoples R China.

年份：2025

卷号：18

起止页码：8447

外文期刊名：JOURNAL OF INFLAMMATION RESEARCH

收录：;Scopus(收录号：2-s2.0-105009531234);WOS:【SCI-EXPANDED(收录号:WOS:001521453100001)】；

基金：This work was supported by Special Project for Emergency of the Ministry of Science and Technology, China (No.2020YFC0845000), Project of Jilin Province Science and Technology Development (No.YDZJ202501ZYTS697) and Project of Jilin Administration of Traditional Chinese Medicine, China (No.2022221).

语种：英文

外文关键词：Qimai Feiluoping decoction; pulmonary fibrosis; network pharmacology; molecular docking; endothelial mesenchymal transition; autophagy

摘要：Purpose: Pulmonary Fibrosis (PF) is a severe interstitial lung disease currently lacking effective prevention strategies. Endothelial mesenchymal transition (EndMT), a novel mechanism for fibroblast production, is closely associated with PF. The precise mechanisms underlying the contribution of EndMT-derived fibroblasts to PF, however, remain unclear. Methods: Using network pharmacology, molecular docking, and molecular dynamics, we identified the key targets and pathways through which Qimai Feiluoping decoction (QM) combats PF. EndMT and autophagy proteins were quantified in bleomycin (BLM)-induced C57BL/6 mice, human umbilical vein endothelial cells (HUVECs), and zebrafish using Western blotting (WB), quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC), immunofluorescence (IF), Transwell migration assays, and transmission electron microscopy (TEM), revealing the targets and pathways through which QM mitigates PF. Results: Network pharmacology, molecular docking, and molecular dynamics suggest that QM combats PF by modulating the PI3K/ AKT/mTOR pathway. Observations from the study indicated that QM was found to alleviate EndMT by restoring autophagy, primarily through inhibition of the PI3K/AKT/mTOR signaling pathway in both BLM-induced C57 mice and HUVECs. Supporting evidence from zebrafish models demonstrated that QM not only counteracts EndMT but also improves a range of vascular functional disorders and remodeling issues following EndMT. Conclusion: Our research validates the active compounds, core targets, and signaling pathways through which QM counters PF, providing valuable insights for its therapeutic application in PF management.