Research on the mechanism of Chaiqi yigan granules against liver cancer via the ferroptosis pathway
- VernacularTitle:柴芪益肝颗粒通过铁死亡途径抗肝癌的作用机制研究
- Author:
Bowen LIU
1
;
Guiping MA
2
;
Feng LI
3
;
Xiaobin LI
4
;
Fenping LU
4
;
Xu PANG
5
;
Shiping HU
4
Author Information
1. Dept. of Preventive Treatment of Disease，Beijing University of Chinese Medicine Shenzhen Hospital （Longgang），Guangdong Shenzhen 518172，China
2. Central Laboratory，Beijing University of Chinese Medicine Shenzhen Hospital （Longgang），Guangdong Shenzhen 518172，China
3. Dept. of Gastroenterology，Nanfang Hospital，Southern Medical University，Guangzhou 510515，China
4. Dept. of Hepatology，Beijing University of Chinese Medicine Shenzhen Hospital （Longgang），Guangdong Shenzhen 518172，China
5. The First School of Clinical Medicine，Beijing University of Chinese Medicine，Beijing 100700，China
- Publication Type:Journal Article
- Keywords:
Chaiqi yigan granules;
liver cancer;
ferroptosis;
mTORC1/SREBP1/SCD1 axis;
network pharmacology
- From:
China Pharmacy
2026;37(10):1272-1276
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the mechanism of Chaiqi yigan granules （CQYG） against liver cancer through the ferroptosis pathway. METHODS Network pharmacology combined with ferroptosis-related database was used to screen key targets and main effective components of CQYG against liver cancer via regulating ferroptosis； molecular docking technology was employed to analyze the binding ability of main active components to key targets. Human liver Huh-7 cells were divided into blank serum control （CON） group， CQYG drug-containing serum （CQYGKL） group， ferroptosis inducer （RSL3） group， mammalian target of rapamycin complex 1 （mTORC1） inhibitor （RMC-5552） group， mTORC1 agonist （CCT007093） group， and CCT007093+CQYGKL group. The levels of Fe 2+ ， malondialdehyde （MDA）， and glutathione （GSH） in the cells were detected in the former three groups； mRNA expressions of mammalian target of rapamycin （mTOR）， sterol regulatory element-binding protein 1 （SREBP1）， and stearoyl-CoA desaturase 1 （SCD1）， protein expressions of SREBP1 and SCD1 as well as phosphorylation levels of mTOR and ribosomal S6 kinase （S6K） proteins were detected in all groups. RESULTS Key targets of CQYG for anti-liver cancer through the ferroptosis pathway were mTOR， SREBP1， SCD1，etc. The main active components included quercetin， tanshinone Ⅱ A ， baicalein， etc. The binding energies of main active components to key targets were all less than －5 kJ/mol. Compared with CON group， the levels of Fe 2+ and MDA in the cells in CQYGKL group and RSL3 group were significantly increased， while the levels of GSH were significantly decreased （ P ＜0.05）. mRNA expressions of mTOR， SREBP1 and SCD1， protein expressions of SREBP1 and SCD1， as well as the phosphorylation levels of mTOR and S6K proteins were significantly decreased in the CQYGKL group， RSL3 group， and RMC-5552 group， whereas all the above indicators were significantly increased in the CCT007093 group （ P ＜0.05）. Compared with CCT007093 group， the changes in all the above indicators were significantly suppressed in the CCT007093+CQYGKL group （ P ＜0.05）. CONCLUSIONS CQYG may induce ferroptosis by inhibiting mTORC1/SREBP1/SCD1 axis， thereby exerting anti-liver cancer effects.
