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阿斯特拉加卢斯多醇通过激活PI3K/AKT/NRF2通路来减轻多克索鲁比诱导的心脏毒性
Xueyang Bai1,2, Hua Wei2, Gangqiong Liu1
1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
PloS one
|February 25, 2025
概括
阿斯特拉加卢斯聚醇 (ASP) 通过通过PI3K/AKT/NRF2通路保护线粒体功能并减少氧化应激,从而防止多克索鲁比诱导的心脏毒性,提供了一种新的治疗策略.
科学领域:
- 心血管药理学心血管药理学
- 分子毒理学 分子毒理学
- 自然产品化学 自然产品化学
背景情况:
- 多克索鲁比 (DOX) 是一种重要的化疗药物,但由于剂量依赖性心脏毒性,其使用受到限制.
- DOX诱导的心脏毒性 (DIC) 涉及氧化应激,线粒体功能障碍和铁,需要心脏保护策略.
研究的目的:
- 调查阿斯特拉加卢斯多 (ASP) 对DOX诱导的心脏毒性的心脏保护作用.
- 阐明PI3K/AKT/NRF2信号通路在ASP的保护机制中的作用.
主要方法:
- 使用AC16和H9C2心肌细胞建立了DOX诱导的心脏毒性模型.
- 评估了细胞活力,线粒体膜潜力 (MMP),活性氧物种 (ROS) 和ANP/BNP表达.
- 研究了PI3K/AKT/NRF2通路激活和通路抑制剂的影响 (LY294002,ML385).
主要成果:
- 治疗ASP显著改善了细胞活力和MMP,同时降低了ROS水平.
- ASP降低了心脏损伤标志物ANP和BNP的调节.
- ASP激活PI3K/AKT/NRF2通路,这对其心脏保护作用至关重要,正如抑制剂研究所证明的那样.
结论:
- 阿斯特拉加卢斯多 (ASP) 显示出对DOX诱导的心脏毒性的显著心脏保护作用.
- ASP通过调节PI3K/AKT/NRF2通路,减轻氧化应激并保持线粒体功能来发挥其保护作用.
- 在接受多克索鲁比化疗的患者中,ASP是预防心脏毒性的有希望的治疗候选者.
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