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黑色素通过通过激活NRF2通路来抑制铁死抑制动脉样硬化

Yangyang Tao¹, Qinglong Zhao², Chengbo Lu³

¹Department of Ultrasound, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|May 23, 2024

概括

黑色素 (MLT) 通过抑制巨细胞铁和激活NRF2通路来减少动脉样硬化,从而抑制Lp-PLA2表达和斑块进展.

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
免疫学免疫学免疫学

背景情况:

黑素 (MLT) 具有有益于心血管健康的抗炎和抗氧化特性.
脂蛋白相关脂酶A2 (Lp-PLA2) 是一种与动脉样硬化风险相关的生物标志物.
了解MLT对Lp-PLA2和动脉样硬化机制的影响至关重要.

研究的目的:

在动脉样硬化期间调查黑素对脂蛋白相关脂酶A2 (Lp-PLA2) 表达的影响.
阐明潜在的分子机制,包括铁和NRF2通路激活.

主要方法:

在体内:ApoE-/-小鼠吃高脂肪饮食,有/没有MLT,评估斑块面积和原.
在体外:用MLT和氧化LDL (ox-LDL) 治疗的巨细胞,测量铁亡标志物,NRF2激活和线粒体功能.
使用铁灭抑制剂/激活剂和NRF2抑制剂 (ML385,AAV-sh-NRF2) 来确认途径的参与.

主要成果:

在小鼠中,MLT的使用显著减少了动脉样硬化斑块的面积,并增加了原蛋白含量.
在巨细胞中,MLT上调了SLC7A11 (xCT) 和谷氨过氧化酶4 (GPX4),增强了抗氧化能力.
MLT激活了NRF2/SLC7A11/GPX4通路,抑制了Lp-PLA2表达,降低了脂质过氧化,并逆转了ox-LDL诱导的铁亡.
抑制NRF2消除了MLT对Lp-PLA2,铁和动脉样硬化的保护作用.

结论:

黑色素通过抑制巨细胞铁和部分激活NRF2通路来减轻动脉样硬化.
MLT抑制Lp-PLA2的表达,为动脉样硬化提供了潜在的治疗策略.

关键词:

抗氧化剂是一种抗氧化剂.动脉样硬化动脉样硬化铁性化 (ferroptosis) 是一种脂蛋白相关的脂酶A2 (Lp-PLA2) 是一种黑激素 (MLT) 的使用

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