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印-3-碳酸通过miR-1271-5p/HDAC9路径抑制巨细胞中的炎症反应和脂质积累

Wei Luo¹, Jun Meng², Xiao-Hua Yu³

¹The First Affiliated Hospital, Department of Cardiology, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Journal of cellular and molecular medicine

|December 19, 2024

概括

印-3-碳酸 (ICA) 通过抑制巨细胞中的脂质积累和炎症来降低动脉样硬化. 它通过激活miR-1271-5p/HDAC9通路来实现这一目标,为其保护作用提供了新的见解.

科学领域:

生物化学生物化学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

动脉样硬化是一种复杂的疾病,涉及脂质积累和巨细胞的炎症.
肠道微生物群中的托芬代谢产物 - - 醇-3-碳酸 (ICA) - - 显示出潜在的动脉保护作用.
基于ICA的动脉保护作用的精确分子机制尚未完全理解.

研究的目的:

研究ICA对THP-1巨细胞衍生的泡细胞中的脂质积累和炎症反应的影响.
为了阐明参与ICA的动脉保护作用的分子通路.

主要方法:

用ICA对THP-1巨细胞进行治疗,以评估其对脂质代谢和炎症的影响.
使用定量实时PCR和西式涂抹测量基因和蛋白质表达水平.
路西法酶记者测定证实了miR-1271-5p和HDAC9.9之间的直接相互作用.

主要成果:

治疗ICA抑制了巨细胞中的脂质积累.
在ICA上调节miR-1271-5p,ABCA1和ABCG1的表达,同时降低HDAC9.
ICA促进了M2巨细胞的两极分化,并减少了炎症性细胞因子IL-6,增加了IL-10.
鉴定出HDAC9是miR-1271-5p的直接标,可以调解ICA的作用.

结论:

通过miR-1271-5p/HDAC9信号通路,ICA抑制脂质积累并减轻巨细胞中的炎症.
这项研究为ICA的动脉保护作用提供了新的分子机制.
ICA代表了动脉样硬化治疗的潜在治疗标.

关键词:

在HDAC9的基础上.美国国际航空公司 (ICA) ICA ICA 动脉样硬化动脉样硬化炎症反应是一种炎症反应.脂质的积累脂质的积累在 miR-1271-5p 中.

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