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已发表论文
四逆汤通过抑制甘草酸依赖的 NF-κB/Akt 通路增强结直肠癌细胞中由半胱氨酸天冬氨酸蛋白酶 3 介导的细胞凋亡
Authors Shi L , Zhang L, Xu J , Guo B
Received 31 July 2025
Accepted for publication 4 October 2025
Published 8 October 2025 Volume 2025:18 Pages 14011—14021
DOI https://doi.org/10.2147/JIR.S557303
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Felix Marsh-Wakefield
Lihao Shi,1,* Ling Zhang,2,* Jiaju Xu,2 Bing Guo2
1Cheeloo College of Medicine, Shandong University, Jinan, 250012, People’s Republic of China; 2Department of Medical Oncology, Taian City Central Hospital, Taian, 271000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Lihao Shi, Cheeloo College of Medicine, Shandong University, Jinan, 250012, People’s Republic of China, Tel +86-0537-2903975, Email lihao_shi_md@163.com
Introduction: Colorectal carcinoma (CRC) is a leading cause of gastrointestinal malignancy worldwide. Its development is closely linked to aberrant activation of NF-κB and Akt signaling pathways. This study aimed to evaluate the inhibitory effects of Compound Sini Decoction (SND), a traditional Chinese medicine, on CRC and clarify its molecular mechanisms.
Methods: An AOM/DSS-induced mouse CRC model was used to assess the in vivo effects of SND. Network pharmacology identified potential targets, while molecular docking and kinetic simulations evaluated binding interactions. In vitro, SND-containing mouse serum was applied to HCT116 and SW480 cells to examine proliferation, migration, apoptosis, ROS production, and signaling pathway modulation.
Results: SND significantly reduced tumor burden, alleviated symptoms, and decreased body weight loss in mice. Network analysis highlighted NFKB1, CASP3, and AKT1 as key targets, suggesting regulation of NF-κB, Caspase-3, and Akt pathways. In vitro, SND inhibited cell proliferation and migration, induced apoptosis, promoted ROS accumulation, suppressed NF-κB and AKT1 phosphorylation, and enhanced CASP3 cleavage. Molecular docking showed Glyuranolide had the strongest binding affinity, particularly with NFKB1 and AKT1, indicating it as a likely effector compound.
Conclusion: SND exerts anti-CRC effects through multi-target synergistic mechanisms involving NF-κB/Akt signaling and Caspase-3-mediated apoptosis. Glyuranolide may represent its key active molecule. These findings provide preliminary evidence supporting SND or its derivatives as potential candidates for precision CRC therapy and suggest a strategy to overcome resistance to single-target treatment. Further studies are warranted to confirm the clinical translational value of SND and the specific role of Glyuranolide.
Keywords: colorectal cancer, Sini decoction, network pharmacology, molecular dynamics simulation, glyuranolide
1Cheeloo College of Medicine, Shandong University, Jinan, 250012, People’s Republic of China; 2Department of Medical Oncology, Taian City Central Hospital, Taian, 271000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Lihao Shi, Cheeloo College of Medicine, Shandong University, Jinan, 250012, People’s Republic of China, Tel +86-0537-2903975, Email lihao_shi_md@163.com
Introduction: Colorectal carcinoma (CRC) is a leading cause of gastrointestinal malignancy worldwide. Its development is closely linked to aberrant activation of NF-κB and Akt signaling pathways. This study aimed to evaluate the inhibitory effects of Compound Sini Decoction (SND), a traditional Chinese medicine, on CRC and clarify its molecular mechanisms.
Methods: An AOM/DSS-induced mouse CRC model was used to assess the in vivo effects of SND. Network pharmacology identified potential targets, while molecular docking and kinetic simulations evaluated binding interactions. In vitro, SND-containing mouse serum was applied to HCT116 and SW480 cells to examine proliferation, migration, apoptosis, ROS production, and signaling pathway modulation.
Results: SND significantly reduced tumor burden, alleviated symptoms, and decreased body weight loss in mice. Network analysis highlighted NFKB1, CASP3, and AKT1 as key targets, suggesting regulation of NF-κB, Caspase-3, and Akt pathways. In vitro, SND inhibited cell proliferation and migration, induced apoptosis, promoted ROS accumulation, suppressed NF-κB and AKT1 phosphorylation, and enhanced CASP3 cleavage. Molecular docking showed Glyuranolide had the strongest binding affinity, particularly with NFKB1 and AKT1, indicating it as a likely effector compound.
Conclusion: SND exerts anti-CRC effects through multi-target synergistic mechanisms involving NF-κB/Akt signaling and Caspase-3-mediated apoptosis. Glyuranolide may represent its key active molecule. These findings provide preliminary evidence supporting SND or its derivatives as potential candidates for precision CRC therapy and suggest a strategy to overcome resistance to single-target treatment. Further studies are warranted to confirm the clinical translational value of SND and the specific role of Glyuranolide.
Keywords: colorectal cancer, Sini decoction, network pharmacology, molecular dynamics simulation, glyuranolide