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铜诱导的亲亡反应及其缓解由奎尔素通过自调节在HEPG2细胞的缓解

Joyeeta Chakraborty¹, Sourav Pakrashi², Jaya Bandyopadhyay¹

¹Maulana Abul Kalam Azad University of Technology, Department of Biotechnology, NH 12, Haringhata, West Bengal 741249, India.

Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)

|August 23, 2024

概括

奎尔是一种多,通过恢复细胞活力和调节细胞亡和自途径,有效地对抗铜诱导的肝脏压力. 这项研究突出显示了奎尔塞丁的存在.

科学领域:

细胞生物学细胞生物学
毒理学毒理学毒理学
营养学科学营养学科学

背景情况:

肝脏容易受到铜 (Cu) 诱导的氧化应激.
奎尔是一种具有抗氧化特性的多,可以防止这种损伤.
这项研究调查了氨酸对HEPG2细胞中铜诱导毒性的保护作用.

研究的目的:

评估奎尔丁在缓解铜诱导的肝毒性方面的疗效.
阐明潜在的细胞机制,包括细胞亡和自.

主要方法:

使用MTT测定评估的细胞活力.
评估了反应性氧物种 (ROS) 水平和线粒体膜潜力 (MMP).
通过显微镜可视化的形态变化;通过西部涂抹分析的apoptotic和自标记物的蛋白质表达.

主要成果:

铜暴露增加了ROS,诱导了形态异常,并破坏了MMP,导致了亡.
铜上调的亲亡蛋白 (PARP,Caspase 3,Bax) 和下调的抗亡蛋白 (Bcl-2). 铜上调的亲亡蛋白 (PARP,Caspase 3,Bax) 和下调的抗亡蛋白 (Bcl-2).
奎尔丁治疗恢复了亡标记物和调节的自蛋白 (LC3II/LC3I转换,p62,HSC 70/90,LAMP-2A,AMPK).

结论:

奎尔西显示出对铜诱导的肝毒性有显著的营养药物潜力.
奎尔素通过影响参与亡和自的关键细胞信号通路来发挥保护作用.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.自自是一种自的过程.铜铜铜铜铜铜这就是HEPG2的目的.奎尔丁 (Quercetin) 是一种青素.这就是ROSOS ROS.

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