国际医药卫生导报 ›› 2025, Vol. 31 ›› Issue (22): 3723-3729.DOI: 10.3760/cma.j.cn441417-20250109-22006

• 基础研究 • 上一篇    下一篇

天香丹颗粒对阿霉素诱导大鼠心肌毒性的保护机制研究

刘冲1  轩辕欢2  沈丹婷3  叶申怡1   

  1. 1温州医科大学附属台州医院精准中心,台州 318050;2新疆医科大学附属中医医院药剂科,乌鲁木齐 830000;3临海市古城街道社区卫生服务中心药剂科,台州 318050
  • 收稿日期:2025-01-09 出版日期:2025-11-01 发布日期:2025-11-19
  • 通讯作者: 叶申怡,Email:yesy@enzemend.com
  • 基金资助:
    浙江省自然科学基金(LTGY23H290007);四川省自然科学基金(23NSFSC1861)

Protective effect of Tianxiangdan Granules against doxorubicin-induced myocardial toxicity in rats

Liu Chong1, Xuanyuan Huan2, Shen Danting3, Ye Shenyi1   

  1. 1 Center of Precision Medicine, Taizhou Hospital Affiliated to Wenzhou Medical University, Taizhou 318050, China; 2 Department of Pharmacy, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi 830000, China; 3 Department of Pharmacy, Linhai Ancient City Community Health Service Center, Taizhou 318050, China
  • Received:2025-01-09 Online:2025-11-01 Published:2025-11-19
  • Contact: Ye Shenyi, Email: yesy@enzemend.com
  • Supported by:
    Natural Science Foundation of Zhejiang Province (LTGY23H290007); Natural Science Foundation of Sichuan Province (23NSFSC1861)

摘要: 目的 探讨天香丹颗粒(TXD)对大鼠阿霉素诱导心肌毒性的保护作用,并深入探究其潜在的作用机制。方法 选取健康的12周龄成年雄性SD大鼠50只,体重200~230 g,分成对照组、阿霉素组和TXD(10、20、40 mg/kg)组。采用阿霉素诱导大鼠心肌毒性模型和H9C2心肌细胞模型,通过检测心功能指标、心肌组织病理HE、透射电子显微镜观察、细胞活力测定TUNEL、活性氧(ROS)水平测定以及线粒体能量代谢相关蛋白表达,分析TXD(10、20、40 mg/kg)对阿霉素诱导心肌毒性的影响。采用单因素方差分析、SNK-q检验进行统计分析。结果 与阿霉素组比较,TXD能显著改善阿霉素诱导的大鼠心肌毒性心功能指标,减轻心肌组织病理学改变,保护心肌细胞线粒体结构,提高心肌细胞活力,并调节细胞凋亡相关蛋白表达。TXD还能降低心肌细胞中的ROS水平,提高Na+、K+-ATPase活性和ATP含量,改善线粒体能量代谢相关蛋白表达。结论 TXD通过介导线粒体能量代谢途径减轻阿霉素诱导的心肌损伤,为临床防治阿霉素心脏毒性和心脏保护提供实验依据。

关键词: 阿霉素, 天香丹颗粒, 心肌毒性, 线粒体能量代谢, 心脏保护, 大鼠

Abstract: Objective To investigate the protective effect of Tianxiangdan Granules (TXD) against doxorubicin (DOX)-induced myocardial toxicity in rats and to explore its potential mechanisms. Methods A total of 50 SD rats, 12 weeks old and 200-230 g in body weight, were divided into a control group, a DOX group, and TXD (10, 20, and 40 mg/kg) pre-treatment groups. The DOX-induced myocardial toxicity models and H9C2 cardiomyocyte models were established. The effects of TXD (10, 20, and 40 mg/kg) against DOX-induced myocardial toxicity were evaluated assessing heart function parameters, myocardial tissue pathology (HE staining), transmission electron microscopy, cell viability (TUNEL assay), reactive oxygen species (ROS) levels, and mitochondrial energy metabolism-related protein expression. One-way analysis of variance and SNK-q test were used for the statistical analysis. Results Compared to the DOX group, TXD could significantly improve the rats' heart function indicators, reduce myocardial tissue pathological changes, protect mitochondrial structure in cardiomyocytes, increase cell viability, and regulate apoptosis-related protein expression. Furthermore, TXD could reduce the ROS level in cardiomyocytes, enhance Na+ and K+-ATPase activity and ATP content, and improve mitochondrial energy metabolism-related protein expression. Conclusion TXD can mediate mitochondrial energy metabolism pathways to alleviate DOX-induced myocardial injury, providing experimental evidences for the clinical prevention and treatment of doxorubicin-induced cardiotoxicity and heart protection.

Key words: Adriamycin, Tianxiangdan , Granules, Cardiac toxicity, Mitochondrial energy metabolism, Cardiac protection, Rat