奇科里提取物通过UCP2/NLRP3通路抑制线粒体损伤,缓解人环素诱导的心脏毒性
Yifei Rao1,2, Yu Wang1, Yadi Liu1
1School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, China.
International journal of molecular sciences
|February 13, 2026
概括
奇科里 (Cichorium intybus L.) 通过减少氧化应激和炎症,有效地预防多克索鲁比诱导的心脏毒性 (DIC). 这项研究确定了香草.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 心血管研究研究心血管研究
- 自然产品化学 自然产品化学
背景情况:
- 德克索鲁比 (Dox) 化疗可以导致严重的心脏毒性 (DIC),导致心力衰竭,治疗选择有限.
- 香草 (Cichorium intybus L.) 具有已知的心脏保护性质,但其对DIC的有效性尚未研究.
研究的目的:
- 评估西瓜在减轻多克索鲁比辛诱导心脏毒性 (DIC) 的治疗潜力.
- 识别活性草化合物并阐明其保护作用中涉及的潜在分子机制.
主要方法:
- 在雄性Sprague-Dawley大鼠中建立了多克索鲁比诱导心脏毒性 (DIC) 模型.
- 香草被用于预防,并评估其对心脏功能和结构的影响.
- 超高性能液态染色学-四极点飞行时间质谱学 (UPLC-QExactivePlus) 和表面等离子体共振 (SPR) 用于识别活性化合物及其与UCP2和NLRP3.3的相互作用.
主要成果:
- 香草的使用显著缓解了Dox诱导的心脏功能障碍,心肌损伤和线粒体损伤.
- 芝麻激活解蛋白2 (UCP2) 和抑制的NOD类受体热蛋白域相关蛋白3 (NLRP3) 信号通路.
- 在老鼠心脏组织中发现了15种草化合物;针对UCP2和NLRP3的9种化合物改善了细胞存活率,减少了氧化应激和炎症,并在Dox处理的H9c2细胞中增强了线粒体功能.
结论:
- 奇科里通过减少氧化应激,炎症和维护线粒体功能,对多克索鲁比诱导的心脏毒性 (DIC) 显示出显著的治疗潜力.
- 该机制涉及UCP2的激活和NLRP3通路的抑制.
- 奇科里代表了一种有前途的基于天然产品的策略,用于预防和治疗多克索鲁比诱导的心脏毒性.
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