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奎瑞通过PACS2/HMOX-1通路抑制铁亡,缓解动脉样硬化中的内皮功能障碍

Hai-Jiao Long¹, Quan-Jun Liu¹, Shi-Ying Qin²

¹Department of Cardiology, The Third Xiangya Hospital of Central South University, Changsha 410000, China.

The American journal of Chinese medicine

|February 15, 2026

概括

奎尔赛丁 (QCT) 通过减少内皮铁,血管损伤的关键驱动器,保护动脉样硬化. 这种饮食中的抗氧化剂调节PACS2-HMOX-1通路,为心血管疾病提供了一个有前途的治疗策略.

科学领域:

心血管研究研究心血管研究
分子生物学分子生物学
营养科学营养科学

背景情况:

动脉样硬化是全球心血管疾病的主要原因之一.
内皮铁性亡日益被认为是血管损伤的一个关键机制.
饮食中的黄类化合物,如奎尔丁 (QCT),具有抗氧化特性,具有潜在的治疗益处.

研究的目的:

为了调查奎尔素 (QCT) 是否能预防动脉样硬化相关的内皮功能障碍.
为了确定QCT是否调节内皮铁.
阐明QCT的保护作用背后的分子机制,重点关注PACS2-HMOX-1通路.

主要方法:

在高脂肪饮食中的ApoE小鼠接受了QCT或ferrostatin-1治疗,以评估斑块负担和稳定性.
人类静脉内皮细胞 (HUVECs) 被暴露在有或没有QCT的氧化低密度脂蛋白 (Ox-LDL) 中,以测量铁亡标记物 (ROS,Fe,HMOX-1).
功能性测试评估了内皮屏障完整性和单细胞粘附;基因调节研究检查了酸酸群分类蛋白2 (PACS2) 表达.

主要成果:

QCT治疗显著减少了大动脉斑块面积,死核大小和巨细胞透,同时改善了小鼠的斑块稳定性.
在体外,QCT通过降低活性氧物种 (ROS) 和铁 (Fe[公式:参见文本]) 水平并降低血红素氧酶-1 (HMOX-1) 的下调抑制了由Ox-LDL诱导的铁.
QCT恢复了内皮完整性,并减少了单细胞粘附,通过机械上调PACS2表达被Ox-LDL抑制.

结论:

奎尔素 (QCT) 通过减轻内皮铁亡,显示出对动脉样硬化有显著的保护作用.
这种机制涉及QCT对PACS2-HMOX-1铁亡途径的调节.
QCT被认为是治疗动脉样硬化和相关血管功能障碍的有前途的饮食抗氧化剂.

关键词:

动脉样硬化是一种动脉样硬化.铁化是铁化的一种.这就是HMOX-1的原因.这就是PACS2的意义.奎尔丁 (Quercetin) 是一种青素.

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