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

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

Ngôn ngữ: eng

Ký hiệu phân loại: 922.945 *Hindus

Thông tin xuất bản: England : Chinese medicine , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 530030

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 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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