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基申颗粒通过通过核红色素因子2相关因子2 (Nrf2) 途径抑制铁化,减轻多克索鲁比诱导的心脏毒性
Siming Xue1, Huan Chen1, Jingmei Zhang1
1School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 100029, China.
Journal of ethnopharmacology
|July 24, 2024
概括
基申颗粒 (QSG) 通过通过核红色素因子2相关因子2 (Nrf2) 途径抑制铁亡来缓解多克索鲁比诱导的心脏毒性 (DIC). 这项研究强调了Nrf2作为DIC的潜在治疗点.
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 多克索鲁比 (DOX) 的使用受心脏毒性限制,心肌细胞铁亡是其中一个关键因素.
- 核红色素因子2相关因子2 (Nrf2) 激活是对抗DOX诱导的心脏毒性 (DIC) 的潜在策略.
- 吉申颗粒 (QSG) 显示出心脏保护作用,但其在DIC中的机制尚不清楚.
研究的目的:
- 为了调查QSG是否通过抑制ferroptosis减轻DIC.
- 为了确定QSG是否通过Nrf2信号通路抑制铁.
主要方法:
- 在体内研究中使用了DIC小鼠模型,评估心脏功能,线粒体损伤,氧化应激 (ROS,GSH,MDA),铁含量和Nrf2通路蛋白质表达.
- 实验室研究探讨了QSG在H9c2细胞中的抗氧化和抗ferroptosis作用,包括Nrf2核转位和Nrf2倒置的影响.
主要成果:
- 在DIC小鼠中,QSG改善了心脏功能,抑制了铁,减少了ROS,铁和MDA,同时增加了GSH.
- QSG保护了线粒体损伤,并促进了Nrf2通路蛋白质的表达,表明耐铁灭症.
- 在体外,QSG表现出抗氧化和抗ferroptosis作用,促进Nrf2核转位;Nrf2干扰减弱了这些保护作用.
结论:
- 通过Nrf2通路抑制铁亡,QSG可以缓解DIC.
- Nrf2成为QSG在预防和治疗DIC的潜在关键治疗标.
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