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凯姆菲罗尔通过Piezo1-介导的MAPK/NF-κB和Nrf2/HO-1信号通路调节巨细胞泡和动脉样硬化

Tianjiao Chu¹, Yuman Wang², Shihao Wang²

¹Innovation Research Institute of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Ji'nan 250355, PR China; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, PR China.

Journal of advanced research

|November 19, 2024

概括

天然抗氧化剂凯姆菲罗尔通过抑制Piezo1通道和流量来预防动脉样硬化,从而减少泡细胞的形成. 这种机制涉及调节炎症因素,氧化应激和关键细胞通路.

科学领域:

心血管研究研究心血管研究
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

动脉样硬化 (AS) 是一种复杂的疾病,其中像kaempferol这样的抗氧化剂显示出希望.
凯费醇发挥其抗动脉样硬化作用的精确机制,特别是在泡细胞形成中,仍然在很大程度上未被定义.

研究的目的:

阐明kaempferol对动脉样硬化的治疗作用背后的分子机制.
研究kaempferol在调节泡细胞积累和相关的炎症和氧化途径中的作用.

主要方法:

在暴露于ox-LDL的巨细胞中研究了kaempferol对炎症因素,CD36,线粒体潜力,ROS,MAPK/NF-κB,Nrf2/HO-1,Ca2+和Piezo1的影响.
使用Piezo1巨特异性淘汰小鼠 (Piezo1ΔLysM) 和ApoE-/-小鼠,包括Piezo1ΔLysM/ApoE-/-组合模型,以评估kaempferol在体内的疗效.

主要成果:

凯姆菲罗尔抑制了炎症,CD36表达,线粒体ROS,Ca2+流入和MAPK/NF-κB信号传递,同时增强了巨细胞中的Nrf2/HO-1.
宏细胞特定的Piezo1枯竭模仿了kaempferol的保护作用,减少了脂质积累和氧化应激.
在体内研究证实了kaempferol减少动脉样硬化斑块,在皮埃佐1贫乏小鼠中有效性降低.

结论:

凯姆菲罗尔抑制了Piezo1介导的Ca2+流入和随后的线粒体ROS产生,从而抑制了泡细胞的形成.
这种机制涉及调节CD36,NF-κB/MAPK和Nrf2/HO-1通路.
凯姆菲罗尔通过向Piezo1通道,代表了动脉样硬化的一种潜在的治疗剂.

关键词:

动脉样硬化是一种动脉样硬化.泡细胞是一种泡细胞.炎症反应是一种炎症反应.凯姆菲罗尔醇是什么意思氧化作用的损伤.这是一个Piezo1.

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