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通过MAPK介导的NFκB亲炎途径和细胞内ROS生成,由3-甲诱导的血管内皮功能障碍

Chien-Ying Lee^1,2, Sheng-Wen Wu^3,4, Jiann-Jou Yang⁵

¹Department of Pharmacology, School of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Rd., Taichung, 402, Taiwan, ROC.

Archives of toxicology

|April 18, 2024

概括

3-Bromofluoranthene (3-BrFlu),一个空气污染物,导致血管内皮功能障碍. 这通过一种促炎途径发生,涉及MAPK和NF-κB,以及增加的活性氧物种 (ROS).

科学领域:

环境毒理学环境毒理学
心血管研究研究心血管研究
分子生物学分子生物学

背景情况:

3-Bromofluoranthene (3-BrFlu) 是一种在空气污染物中发现的多环芳香碳化合物代谢物.
内皮功能障碍是心血管和血管疾病的关键因素.
3-BrFlu对内皮功能障碍的影响的分子机制尚不清楚.

研究的目的:

在体内和体外研究3-Bromofluoranthene (3-BrFlu) 对血管内皮功能障碍的分子机制.
阐明炎症途径,反应性氧物种和抗氧化剂反应在3-BrFlu诱导的内皮损伤中的作用.

主要方法:

斑马鱼模型被用来评估体内血管的影响,如血管生成和大动脉扩张.
在体外研究中使用SVEC4-10细胞来检查血管内皮的完整性和透性.
分子分析包括测量炎症媒介 (PGE2,TNFα,IL-6),酶表达 (COX2),信号通路 (MAPK,NF-κB),活性氧物种 (ROS) 和抗氧化酶 (SOD,催化酶,HO-1,Nrf-2).

主要成果:

在斑马鱼中,3-BrFlu诱导了度依赖的宫外血管生成和大动脉扩张.
在体外,3-BrFlu破坏了内皮完整性,并通过促炎反应增加了透性,包括COX2表达和随后的PGE2生成.
3-BrFlu激活了MAPK介导的NFκB通路,导致TNFα和IL-6的增加,并且还诱导了细胞内ROS生成,降低了抗氧化酶的调节.
虽然Nrf-2调节了抗氧化酶 (HO-1) 的上调,但这并没有扭转内皮功能障碍.

结论:

3-Bromofluoranthene (3-BrFlu) 是一种危险的空气污染物,可诱导血管内皮功能障碍.
该机制涉及MAPK介导的NFκB亲炎途径和细胞内ROS生成.
通过3-BrFlu对抗氧化酶的升级并不能防止对血管内皮的有害影响.

关键词:

3 - 二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二二抗氧化酶是一种抗氧化酶.这就是HO-1的HO-1.这就是MAPKK的意思.在 NFκBB 的情况下.在 Nrf-2 中.这就是ROSOS ROS.血管内皮功能障碍血管内皮功能障碍

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