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维素对通过Keap1/Nrf2-依赖信号通路对IL-17诱导的血管内皮炎的保护作用

Ting Gan¹, Qian Xing¹, Nan Li¹

¹State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, Jiangxi, 330047, China.

Molecular nutrition & food research

|February 1, 2024

概括

维素是一种天然化合物,通过激活Nrf2通路,有效降低血管炎症. 这项研究确定了Nrf2作为vitaxin的关键标.

科学领域:

生物化学生物化学
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

在各种食物中发现的一种C-糖基化类黄类物质Vitexin具有潜在的健康益处.
维捷辛有益作用的精确分子标,特别是血管健康方面,尚不清楚.
血管低度炎症是导致心血管疾病的重要因素.

研究的目的:

建立一个可靠的体外细胞模型来研究血管低度炎症.
阐明维特辛在血管内皮细胞中的抗炎作用机制.
确定维特辛通过哪些分子点来发挥其抗炎作用.

主要方法:

在人静脉内皮细胞 (HUVEC) 中使用低剂量瘤亡因子-α (TNFα) 和介质蛋白-17 (IL-17) 的血管低级炎症模型的开发.
研究维捷辛对炎症性细胞因子表达,反应性氧物种 (ROS) 生产和核因素红色素2相关因子2 (Nrf2) 激活的影响.
使用了包括Nrf2敲击,表面等离子体共振 (SPR),药物亲和度响应目标稳定性 (DARTS) 和分子对接在内的技术来识别维特辛的直接目标.
在小鼠体内验证,使用口服测量和高脂肪食补充剂,以评估维捷辛在血管中的生物可用性和抗炎疗效.

主要成果:

联合低剂量的TNFα和IL-17有效诱导血管炎症,而不会增加氧化应激或ROS.
维素被HUVEC细胞吸收,导致Nrf2蛋白水平增加,并随后减轻了炎症.
维捷辛的抗炎作用依赖于Nrf2,这是通过敲击实验证明的.
SPR,DARTS和分子对接证实,维特辛直接与凯尔奇类ECH相关蛋白1 (Keap1) 结合,破坏Keap1-Nrf2相互作用并激活Nrf2.
在体内研究显示,小鼠的血液中维特辛水平增加,Nrf2激活,血管炎症改善.

结论:

成功建立了一个强大的体外细胞模型用于血管低级炎症.
维素直接准Keap1,激活Nrf2通路,从而抑制血管炎症.
Nrf2被确定为一个关键的分子点,在血管内皮中调解维特辛的抗炎作用.

关键词:

Nrf2 没有任何问题.药物亲和度响应性目标稳定性目标稳定性这是一种轻度炎症.吸收吸收吸收吸收血管内皮细胞是血管内皮细胞.维特克辛 (Vitexin) 是一种快速的药物

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