中国药物警戒 ›› 2025, Vol. 22 ›› Issue (2): 121-127.
DOI: 10.19803/j.1672-8629.20230658

• 专家论坛 • 上一篇    下一篇

雷公藤甲素肝损伤研究进展

唐千茴1, 张昊然1, 张陆勇1,2,*, 江振洲1,3#   

  1. 1中国药科大学新药筛选中心,江苏 南京 210009;
    2广东药科大学新药研发中心,广东 广州 510006;
    3江苏省药效研究与评价服务中心,江苏 南京 210009
  • 收稿日期:2023-10-24 出版日期:2025-02-17 发布日期:2025-02-17
  • 通讯作者: *张陆勇,男,博士,教授·博导,分子药理与毒理学。E-mail:lyzhang@cpu.edu.cn;#为共同通信作者。
  • 作者简介:唐千茴,女,在读博士,药理学; 张陆勇,二级教授,博士生导师,广东药科大学原副校长,中国药科大学国家南京新药筛选中心主任; 第十一届、十二届药典委员会委员,全国药学专业学位研究生教育指导委员会委员,“十三五”“十四五”国家重点研发计划“中医药现代化研究”重点专项专家组成员,国家药品监督管理局中药管理战略决策专家咨询委员会委员,教育部新世纪优秀人才,享受国务院政府特殊津贴专家; 研究方向为新药筛选、早期成药性评价及药物毒理学; 主持完成国家自然科学基金国际(地区)合作与交流重大项目、重大新药创制等40多项国家及省部级科研项目; 已发表SCI论文249篇,H指数61; 申请专利175件,获授权84件; 参与研发的新药项目获新药证书9项,临床批件31项; 获江苏省科技进步一等奖、教育部科技进步二等奖、山东省科技进步一等奖、江苏省教育教学与研究成果奖(研究类)二等奖等奖项; 《中国药物警戒》期刊编委
  • 基金资助:
    国家自然科学基金资助项目(82274200、82074114、81973562、81773995)

Research Progress in Triptolide-Induced Live Injury

TANG Qianhui1, ZHANG Haoran1, ZHANG Luyong1,2,*, JIANG Zhenzhou1,3#   

  1. 1New Drug Screening Center, China Pharmaceutical University, Nanjing Jiangsu 210009, China;
    2Center for Drug Research and Development, Guangdong Pharmaceutical University, Guangzhou Guangdong 510006, China;
    3Jiangsu Center for Pharmacodynamics Research and Evaluation, Nanjing Jiangsu 210009, China
  • Received:2023-10-24 Online:2025-02-17 Published:2025-02-17

摘要: 目的 总结雷公藤甲素肝毒性机制的相关研究,为了解雷公藤甲素诱发药物性肝损伤的机制提供依据。方法 通过文献检索与分析,从直接毒性和间接毒性两方面总结雷公藤甲素诱发药物性肝损伤的机制。结果 雷公藤甲素肝毒性机制涉及肝细胞氧化应激、线粒体损伤、代谢异常、NKT细胞激活、辅助性T淋巴细胞与调节性T淋巴细胞失衡、肝脏对炎性刺激的敏感性增加等。结论 雷公藤甲素肝毒性机制复杂,直接毒性作用靶点广泛,间接毒性具有更强的隐匿性和复杂性,雷公藤甲素肝毒性的研究可为雷公藤及其制剂的增效减毒以及临床安全合理用药提供理论参考。

关键词: 雷公藤, 雷公藤甲素, 肝损伤, 肝毒性, 直接毒性, 间接毒性, 机制研究

Abstract: Objective To summarize the research progress in the hepatotoxicity mechanism of triptolide and shed light on the mechanism of drug-induced liver injury caused by triptolide. Methods Based on literature research, the mechanism of drug induced liver injury caused by triptolide was summarized in terms of direct toxicity and indirect toxicity. Results The hepatotoxic mechanism of triptolide involved oxidative stress, mitochondrial damage, metabolic abnormalities, activation of NKT cells, imbalance between T helper cells and regulatory T cells, and increased liver sensitivity to inflammatory stimuli. Conclusion The hepatotoxicity mechanism of triptolide is complex, as there are a wide range of targets for direct toxicity. In addition, the indirect toxicity is highly concealed and complex. The elucidation of mechanisms of hepatotoxicity caused by triptolide provides a reference for enhancing the efficacy and reducing the toxicity of Tripterygium wilfordii Hook.f. and its preparations as well as for clinical safety and rational drug use.

Key words: Tripterygium wilfordii Hook.f., Triptolide, Liver Injury, Hepatotoxicity, Direct Toxicity, Indirect Toxicity, Hepatotoxicity Mechanism

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