文献类型：期刊文献

英文题名：Network pharmacology and UHPLC-HRMS reveal the mechanism of QSFZYL and BMSCs overexpressing IFN-γ against lung adenocarcinoma

作者：Lv, Zhen[1];Liu, MingXuan[1];Yang, YingYing[1];Xie, YaHui[1];Tian, YiHong[1];Xu, XiangNing[1];Wang, YinDi[1];Wei, XingMing[1];Ma, DongJing[1];Tian, XueJiao[1];Wu, JianJun[1]

第一作者：Lv, Zhen

通信作者：Wu, JJ[1]

机构：[1]Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou, Gansu, Peoples R China

第一机构：甘肃中医药大学公共卫生学院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou, Gansu, Peoples R China.|[10735e9d5e7087247e71b]甘肃中医药大学公共卫生学院;[10735]甘肃中医药大学;

年份：2025

卷号：16

外文期刊名：FRONTIERS IN IMMUNOLOGY

收录：;Scopus(收录号：2-s2.0-105010873209);WOS:【SCI-EXPANDED(收录号:WOS:001524698200001)】；

基金：The author(s) declare that financial support was received for the research and/or publication of this article. This work was supported by National Natural Science Foundation of China (grant no. 82160900), the Youth Science and Technology Foundation Project of Gansu Province (grant no.23JRRA1730 and grant no.23JRRA1726) and the 2022 Annual Innovation Fund Project of Gansu Provincial Universities (grant no.2022B-119).

语种：英文

外文关键词：BMSCs; IFN-gamma; JAK/STAT; UHPLC-HRMS; lung adenocarcinoma; network pharmacology

摘要：Background Lung cancer is a significant public health concern in China, posing a serious threat to the population. The QiShenFuZhengYiLiu (QSFZYL) is commonly prescribed as a complementary treatment for cancer patients, although its anticancer mechanism remains unclear. The purpose of this study was to explore the therapeutic mechanisms of QSFZYL in lung adenocarcinoma (LUAD).Methods The mechanism of QSFZYL for treating LUAD was analyzed using comprehensive network pharmacology and UHPLC-HRMS, combined with experimental validation (in vivo).Results Network pharmacology analysis suggested that the therapeutic effects of QSFZYL on LUAD may involve the JAK/STAT signaling pathway. UHPLC-HRMS identified 26 differential components, with representative compounds including astragalus lysine alkaloids, monoterpenoids, isoflavonoids, and flavonoids. In vivo experiments demonstrated that QSFZYL combined with IFN-gamma significantly inhibited LUAD growth and promoted infiltration of CD3 and CD8 T cell, and downregulated JAK2, STAT3, and PD-L1 expression, promoted apoptosis.Conclusion QSFZY combined with IFN-gamma overexpressing BMSCs effectively inhibit LUAD progression. The primary mechanisms include the suppression of cancer cell growth, promotion of apoptosis and infiltration of CD3 and CD8 T cells, and inhibition of the JAK2/STAT3 signaling pathway, and downregulated PD-L1 expression.