文献类型：期刊文献

英文题名：Licoricesaponin G2 ameliorates bleomycin-induced pulmonary fibrosis via targeting TNF-α signaling pathway and inhibiting the epithelial-mesenchymal transition

作者：Ma, Jing[1];Ding, Lu[2,3];Zang, Xiaoyu[1];Wei, Ruonan[4];Yang, Yingying[5];Zhang, Wei[6];Su, Hang[2];Li, Xueyan[7];Li, Min[7];Sun, Jun[1];Zhang, Zepeng[2,3];Wang, Zeyu[2];Zhao, Daqing[2];Li, Xiangyan[2];Zhao, Linhua[8];Tong, Xiaolin[1,8]

第一作者：Ma, Jing

通信作者：Tong, XL[1];Li, XY[2];Zhao, LH[3];Tong, XL[3]

机构：[1]Changchun Univ Chinese Med, Coll Tradit Chinese Med, Changchun, Peoples R China;[2]Changchun Univ Chinese Med, Northeast Asia Res Inst Tradit Chinese Med, Key Lab Act Subst & Biol Mech Ginseng Efficacy, Jilin Prov Key Lab Biomacromolecules Chinese Med, Changchun, Peoples R China;[3]Changchun Univ Chinese Med, Coll Tradit Chinese Med, Res Ctr Tradit Chinese Med, Changchun, Peoples R China;[4]Shiyan Hosp Tradit Chinese Med, Shiyan, Peoples R China;[5]China Japan Friendship Hosp, Natl Ctr Integrated Tradit Chinese Med & Western M, Beijing 100029, Peoples R China;[6]Gansu Univ Chinese Med, Sch Basic Med, Lanzhou, Peoples R China;[7]Changchun Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Changchun, Peoples R China;[8]China Acad Chinese Med Sci, GuangAnmen Hosp, Inst Metab Dis, Beijing, Peoples R China

第一机构：Changchun Univ Chinese Med, Coll Tradit Chinese Med, Changchun, Peoples R China

通信机构：[1]corresponding author), Changchun Univ Chinese Med, Coll Tradit Chinese Med, Changchun, Peoples R China;[2]corresponding author), Changchun Univ Chinese Med, Northeast Asia Res Inst Tradit Chinese Med, Key Lab Act Subst & Biol Mech Ginseng Efficacy, Jilin Prov Key Lab Biomacromolecules Chinese Med, Changchun, Peoples R China;[3]corresponding author), China Acad Chinese Med Sci, GuangAnmen Hosp, Inst Metab Dis, Beijing, Peoples R China.

年份：2024

卷号：15

外文期刊名：FRONTIERS IN PHARMACOLOGY

收录：;Scopus(收录号：2-s2.0-85204462225);WOS:【SCI-EXPANDED(收录号:WOS:001315349400001)】；

基金：The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by Special Project for Emergency of the Ministry of Science and Technology, China (No. 2020YFC0845000), Jilin Province Science and Technology Development, China (Nos YDZJ202301ZYTS136 and YDZJ202CXJD049) and Plan Project and Project of Jilin Administration of Traditional Chinese Medicine, China (No. 2022221).

语种：英文

外文关键词：licoricesaponin G2; pulmonary fibrosis; epithelial-mesenchymal transition; TNF-alpha signaling pathway; network analysis

摘要：Background Pulmonary fibrosis (PF) emerges as a significant pulmonary sequelae in the convalescent phase of coronavirus disease 2019 (COVID-19), with current strategies neither specifically preventive nor therapeutic. Licoricesaponin G2 (LG2) displays a spectrum of natural activities, including antibacterial, anti-inflammatory, and antioxidant properties, and has been effectively used in treating various respiratory conditions. However, the potential protective effects of LG2 against PF remain underexplored.Methods Network analysis and molecular docking were conducted in combination to identify the core targets and pathways through which LG2 acts against PF. In the model of bleomycin (BLM)-induced C57 mice and transforming growth factor-beta 1 (TGF-beta 1)-induced A549 and MRC5 cells, techniques such as western blot (WB), quantitative Real-Time PCR (qPCR), Immunohistochemistry (IHC), Immunofluorescence (IF), and Transwell migration assays were utilized to analyze the expression of Epithelial-mesenchymal transition (EMT) and inflammation proteins. Based on the analysis above, we identified targets and potential mechanisms underlying LG2's effects against PF.Results Network analysis has suggested that the mechanism by which LG2 combats PF may involve the TNF-alpha pathway. Molecular docking studies have demonstrated a high binding affinity of LG2 to TNF-alpha and MMP9. Observations from the study indicated that LG2 may mitigate PF by modulating EMT and extracellular matrix (ECM) remodeling. It is proposed that the therapeutic effect is likely arises from the inhibition of inflammatory expression through regulation of the TNF-alpha pathway.Conclusion LG2 mitigates PF by suppressing TNF-alpha signaling pathway activation, modulating EMT, and remodeling the ECM. These results provide compelling evidence supporting the use of LG2 as a potential natural therapeutic agent for PF in clinical trials.