中国药物警戒 ›› 2026, Vol. 23 ›› Issue (10): 1189-1194.
DOI: 10.19803/j.1672-8629.20260540

• 综述 • 上一篇    下一篇

麦冬皂苷D活性成分与毒性杂质研究进展

黄颖1, 张丽君1, 梅诗棋2, 张娴勰2#, 王宇光1,2*   

  1. 1天津中医药大学中医药研究院,天津 301617;
    2军事科学院军事医学研究院,北京 100850
  • 收稿日期:2026-07-01 出版日期:2026-10-15 发布日期:2026-10-16
  • 通讯作者: *王宇光,男,博士,研究员·博导,高原心脏病与辐射防治。E-mail: 13611317940@139.com。#为共同通信作者。
  • 作者简介:黄颖,女,在读硕士,高原心脏病。
  • 基金资助:
    国家自然科学基金资助项目(82474196)

Research progress in active components and toxic impurities of ophiopogonin D

Huang Ying1, Zhang Lijun1, Mei Shiqi2, Zhang Xianxie2#, Wang Yuguang1,2*   

  1. 1Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China;
    2Academy of Military Medical Sciences, Academy of Military Sciences, Beijing 100850, China
  • Received:2026-07-01 Online:2026-10-15 Published:2026-10-16

摘要: 目的 系统综述麦冬皂苷D(OPD)治疗高原心脏病的药效基础与作用机制,梳理其与同分异构体麦冬皂苷D′(OPD′)的毒性特征,为麦冬皂苷类成分在高原心脏病中的安全合理应用提供参考。方法 探究麦冬皂苷D的心血管保护机制、麦冬皂苷D′毒性机制、OPD与OPD′相互作用等研究,并对其进行归纳、分析、总结。结果 OPD可通过CYP2J3/EETs系统及抗炎、抗凋亡、抗氧化等多重机制发挥心肌保护作用。在模拟海拔6 000 m的低压缺氧动物模型中,OPD可显著降低心肌酶谱及损伤标志物水平,提高超氧化物歧化酶(SOD)活力,减轻心肌组织病理损伤。然而,OPD′具有明显的细胞毒性和溶血毒性,含麦冬制剂中OPD′的含量测定已成为质量控制的关键指标。急性毒性试验提示,先给予OPD可有效降低OPD′的急性毒性。结论 目前OPD在高原心肌保护方面已取得一定药效学研究进展,但在OPD′的毒性特征认识及含麦冬制剂质量控制仍存在不足。未来应系统阐明OPD与OPD′的相互作用机制,建立兼顾药效与安全的质量控制标准,为麦冬皂苷类成分在高原心脏病中的安全应用提供参考。

关键词: 麦冬皂苷D, 麦冬皂苷D′, 高原心脏病, 心肌保护, 毒性, 质量控制

Abstract: Objective To summarize the pharmacology and mechanisms of action of Ophiopogonin D (OPD) against high-altitude heart disease, and review the toxicological profile and current assessment of risks of its isomer, Ophiopogonin D′ (OPD′), in order to provide a reference for safe and rational application of ophiopogonin saponins. Methods Studies on the cardioprotective mechanisms of OPD, animal experiments on high-altitude myocardial injury, the cytotoxicity and hemolytic toxicity of OPD′, and the drug-drug interactions between OPD and OPD′ were reviewed. The findings from these studies were analyzed. Results OPD exerted cardioprotective effects through such mechanisms as the CYP2J3/EETs pathway and anti-inflammatory, anti-apoptotic and antioxidant actions. In an animal model of hypobaric hypoxia that simulated an altitude of 6000 m, OPD significantly reduced myocardial enzyme levels and biomarkers of injury, enhanced SOD activity, and attenuated myocardial histopathological damage. However, OPD′ evoked significant cytotoxicity and hemolytic toxicity, making the control of OPD′ contents in Ophiopogon japonicus-containing formulations critical to quality optimization. Acute toxicity studies found that OPD, when used before OPD′, could effectively reduce the acute toxicity of OPD′. Conclusion So far, progress has been made in research on the pharmacodynamics of OPD against high-altitude myocardial injury, but the toxicological profile of OPD′ and quality control of Ophiopogon japonicus-containing formulations remains to be investigated. Subsequent studies should elucidate the interactions between OPD and OPD′, and establish quality control standards that balance therapeutic efficacy with safety so as to facilitate the application of ophiopogonin saponins in high-altitude heart disease.

Key words: Ophiopogonin D, Ophiopogonin D′, High-Altitude Heart Disease, Cardioprotection, Toxicity, Quality Control

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