Study on mechanism of stigmasterol inhibiting hepatocellular carcinoma based on TLR4/MyD88/NF-κB signaling pathway
- VernacularTitle:基于TLR4/MyD88/NF-κB信号通路探讨豆甾醇抗肝细胞癌的作用机制
- Author:
Chun YU
1
;
Yan-hua MA
1
Author Information
- Publication Type:Journal Article
- Keywords: stigmasterol; Toll-like receptor 4; myeloid differentiation primary response gene 88; nuclear fac-tor-KB; hepatocellular carcinoma; apoptosis
- From: Chinese Pharmacological Bulletin 2025;41(5):867-873
- CountryChina
- Language:Chinese
- Abstract: Aim To utilize molecular docking and in vitro experiments to investigate the regulatory mecha-nism of stigmasterol on the TLR4/MyD88/NF-κB sig-naling pathway in hepatocellular carcinoma.Methods Molecular docking was performed using AutoDock to study the binding affinity of stigmasterol with TLR4,MyD88,and NF-κB.The effects on cell proliferation and migration were assessed through CCK-8,wound healing assays,and Transwell experiments,while colony formation ability was measured using a colony formation assay.Flow cytometry was employed to examine apop-tosis and cell cycle.Western blot analysis was used to evaluate the expression levels of TLR4,MyD88,and NF-κB proteins after stigmasterol treatment.Results Molecular docking indicated that stigmasterol exhibited favorable binding conformations with TLR4,MyD88,and NF-κB.In vitro,stigmasterol demonstrated inhibi-tory effects on proliferation,migration,invasion,and colony formation in hepatocellular carcinoma cells.Ad-ditionally,it promoted apoptosis,inhibited cell cycle progression,and reduced protein expression of the TLR4/MyD88/NF-κB signaling pathway(P＜0.05).Conclusion Stigmasterol suppresses the activity of hepatocellular carcinoma cells by modulating the TLR4/MyD88/NF-κB signaling pathway.
