数字农科院2.0

Huqi formula suppresses hepatocellular carcinoma growth by modulating the PI3K/AKT/mTOR pathway and promoting T cell infiltration

文献类型： 外文期刊

作者： Donghao Yin;Xiang Li;Xuemeng Yang;Xiaofei Shang;Zhen Li;Jiahao Geng;Yanyu Xu;Zijing Xu;Zixuan Wang;Zimeng Shang;Zhiyun Yang;Linlan Hu;Quanwei Li;Jiabo Wang;Xinhua Song;Xiuhui Li;Xiaojun Wang

作者机构：

关键词： Apoptosis;Hepatocellular carcinoma;Huqi formula;Immunotherapy;T cells

期刊名称： Chinese Medicine (United Kingdom)

ISSN： 1749-8546

年卷期： 2025 年 20 卷 1 期

页码：

收录情况： SCIE（2025版）

摘要： Background: Hepatocellular carcinoma (HCC) poses ongoing difficulties for public health systems due to its high incidence and poor prognosis. Huqi formula (HQF), a well-known prescription in traditional Chinese medicine, has demonstrated notable clinical effectiveness in the treatment of HCC. However, the mechanisms underlying its therapeutic effects have yet to be completely elucidated. Purpose: This study aimed to investigate the anti-HCC effects of HQF and its underlying mechanisms. Methods: Chemical profiling and quantification of HQF were conducted by LC–MS and HPLC. Orthotopic and subcutaneous tumor models were established through hydrodynamic injection of Akt/Nras plasmids and subcutaneous injection of c-Met/sgPten cells, respectively, to evaluate the therapeutic effects of HQF on HCC. Network pharmacology, RNA-Seq, molecular docking, Western blot, and flow cytometry were employed to assess the anti-HCC mechanisms. Results: LC–MS analysis identified 41 components, with HPLC quantification showing salvianolic acid B as the most abundant compound (0.303%). In Akt/Nras and c-Met/sgPten-induced HCC models, HQF significantly reduced tissue damage, improved liver function, and inhibited HCC progression. Mechanistic studies revealed that HQF induced apoptosis in HCC cells by downregulating p-PI3K, p-AKT, and p-mTOR expression, with molecular docking indicating the strongest binding affinity between salvianolic acid B and PI3K. HQF further enhanced CD4+ and CD8+ T cell infiltration within the tumor microenvironment. When combined with PD-1 therapy, HQF improved therapeutic efficacy against HCC. Finally, toxicity assays confirmed the safety profile of HQF. Conclusion: HQF demonstrated significant anti-HCC effects and a synergistic effect with PD-1, could be used as an alternative therapeutic agent for HCC.

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