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柴芪益肝颗粒通过铁死亡途径抗肝癌的作用机制研究
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| 篇名： | 柴芪益肝颗粒通过铁死亡途径抗肝癌的作用机制研究 |
| TITLE： | Research on the mechanism of Chaiqi yigan granules against liver cancer via the ferroptosis pathway |
| 摘要： | 目的 探讨柴芪益肝颗粒通过铁死亡途径抗肝癌的作用机制。方法采用网络药理学方法，结合铁死亡数据库，筛选柴芪益肝颗粒调控铁死亡抗肝癌的关键靶点与主要有效成分；运用分子对接技术分析主要有效成分与关键靶点的结合能力。将人肝癌Huh-7细胞分为空白血清对照（CON）组、柴芪益肝颗粒含药血清（CQYGKL）组、铁死亡诱导剂（RSL3）组、哺乳动物雷帕霉素靶蛋白复合物1（mTORC1）抑制剂（RMC-5552）组、mTORC1激动剂（CCT007093）组及CCT007093+CQYGKL组，检测前3组细胞中Fe2+、丙二醛（MDA）及谷胱甘肽（GSH）水平，所有组细胞中哺乳动物雷帕霉素靶蛋白（mTOR）、哺乳动物固醇调节元件结合蛋白1（SREBP1）、硬脂酰辅酶A去饱和酶1（SCD1）mRNA表达和SREBP1、SCD1蛋白表达以及mTOR、核糖体S6激酶（S6K）蛋白磷酸化水平。结果柴芪益肝颗粒通过铁死亡途径抗肝癌的关键靶点有mTOR、SREBP1、SCD1等，主要有效成分有槲皮素、丹参酮ⅡA、黄芩素，主要有效成分与关键靶点的结合能均小于－5kJ/mol。与CON组比较，CQYGKL组和RSL3组细胞中Fe2+、MDA水平均显著升高，GSH水平均显著降低（P＜0.05）；CQYGKL组、RSL3组、RMC-5552组细胞中mTOR、SREBP1、SCD1mRNA表达量和SREBP1、SCD1蛋白表达量以及mTOR、S6K蛋白磷酸化水平均显著降低，CCT007093组细胞中上述指标均显著升高（P＜0.05）。而相较CCT007093组，CCT007093+CQYGKL组细胞的上述指标变化均被显著抑制（P＜0.05）。结论柴芪益肝颗粒可能通过抑制mTORC1/SREBP1/SCD1轴诱导铁死亡，从而发挥抗肝癌作用。 |
| 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. |
| 期刊： | 2026年第37卷第10期 |
| 作者： | 刘博文；马贵萍；李峰；李晓斌；卢芬萍；庞旭；胡世平 |
| AUTHORS： | LIU Bowen，MA Guiping，LI Feng，LI Xiaobin，LU Fenping，PANG Xu，HU Shiping |
| 关键字： | 柴芪益肝颗粒；肝癌；铁死亡；mTORC1/SREBP1/SCD1轴；网络药理学；分子对接 |
| KEYWORDS： | Chaiqi yigan granules； liver cancer； ferroptosis； mTORC1/SREBP1/SCD1 axis； network pharmacology； |
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