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通过SIRT6/Nrf2信号传递,CTRP4可以缓解炎症,从而减轻HUVECs与THP-1单细胞之间的相互作用

Jaw Long Sun¹, Jae Hak Ryu¹, Wonjun Cho¹

¹Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.

Biochemical and biophysical research communications

|November 28, 2023

概括

心脏类型细胞因子B123 (CTRP4) 在高脂血症中减少炎症和细胞粘附. CTRP4通过SIRT6/Nrf2通路改善内皮细胞-单细胞相互作用,为与肥胖相关的动脉样硬化治疗提供了潜力.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
心血管研究研究心血管研究

背景情况:

心脏类型细胞因子B123 (CTRP4) 是一种具有已知的抗炎和抗肥胖作用的阿迪波金.
超脂血症可以加剧炎症并改变内皮细胞与单细胞的相互作用,导致动脉样硬化.
了解CTRP4在这些过程中的作用对于开发有针对性的疗法至关重要.

研究的目的:

为了研究CTRP4对炎症和内皮细胞-单细胞相互作用在高脂血症条件下的影响.
阐明CTRP4的作用背后的分子机制,特别关注SIRT6/Nrf2通路.

主要方法:

西方涂抹用于分析人类静脉内皮细胞 (HUVEC) 和THP-1单细胞中的蛋白质表达.
实验涉及将细胞暴露在超脂性疾病中,并用CTRP4.4治疗它们.
使用RNA干扰 (siRNA) 来抑制SIRT6和Nrf2的表达.

主要成果:

CTRP4治疗显著减少了THP-1单细胞与HUVECs的附着.
在超脂血细胞中,CTRP4降低了粘附分子和炎症标记物的表达.
CTRP4增加了SIRT6的表达,并促进了Nrf2的核转位.
沉默SIRT6或Nrf2消除了CTRP4.4的有益作用.

结论:

通过改善内皮细胞与单细胞的相互作用,CTRP4具有抗炎作用.
CTRP4的保护作用通过SIRT6/Nrf2依赖途径进行介导.
CTRP4代表了管理与肥胖相关的动脉样硬化的潜在治疗标.

关键词:

动脉样硬化是一种动脉样硬化.在CTRP4中使用.在HUVECEC中使用.Nrf2 没有任何问题.在SIRT6上.这就是THP-1的特点.

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