Lv Zhen, Liu MingXuan, Yang YingYing, Xie YaHui, Tian YiHong, Xu XiangNing, Wang YinDi, Wei XingMing, Ma DongJing, Tian XueJiao, Wu JianJun
School of Public Health, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Front Immunol. 2025 Jun 26;16:1593121. doi: 10.3389/fimmu.2025.1593121. eCollection 2025.
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).
The mechanism of QSFZYL for treating LUAD was analyzed using comprehensive network pharmacology and UHPLC-HRMS, combined with experimental validation ().
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. experiments demonstrated that QSFZYL combined with IFN-γ significantly inhibited LUAD growth and promoted infiltration of CD3 and CD8 T cell, and downregulated JAK2, STAT3, and PD-L1 expression, promoted apoptosis.
QSFZY combined with IFN-γ 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.
肺癌在中国是一个重大的公共卫生问题，对民众构成严重威胁。启神扶正抑瘤（QSFZYL）通常被用作癌症患者的辅助治疗药物，但其抗癌机制尚不清楚。本研究的目的是探讨QSFZYL在肺腺癌（LUAD）中的治疗机制。
采用综合网络药理学和超高效液相色谱-高分辨质谱联用技术，并结合实验验证，分析QSFZYL治疗LUAD的机制。
网络药理学分析表明，QSFZYL对LUAD的治疗作用可能涉及JAK/STAT信号通路。超高效液相色谱-高分辨质谱联用技术鉴定出26种差异成分，代表性化合物包括黄芪赖氨酸生物碱、单萜类、异黄酮类和黄酮类。实验表明，QSFZYL联合IFN-γ可显著抑制LUAD生长，促进CD3和CD8 T细胞浸润，下调JAK2、STAT3和PD-L1表达，促进细胞凋亡。
QSFZY联合过表达IFN-γ的骨髓间充质干细胞可有效抑制LUAD进展。主要机制包括抑制癌细胞生长、促进细胞凋亡和CD3及CD8 T细胞浸润、抑制JAK2/STAT3信号通路以及下调PD-L1表达。
