Motorcycle exhaust particles up-regulate expression of vascular adhesion molecule-1 and intercellular adhesion molecule-1 in human umbilical vein endothelial cells

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• 作者：Chen-Chen Lee^a ; Shih-Hsuan Huang^b ; Ya-Ting Yang^b ; Yu-Wen Cheng^c ; Ching-Hao Li^b ; Jaw-Jou Kang^b ; ^{jjkang@ntu.edu.tw}
• 关键词：Motorcycle exhaust particle ; Polycyclic aromatic hydrocarbons ; Cell adhesion molecule ; Oxidative stress ; NF-魏B
• 刊名：Toxicology in Vitro
• 出版年：2012
• 期刊代码：48_08872333
• 类别：pha
• 出版时间：June, 2012
• 卷：26
• 期：4
• 页码：552-560
• 文件大小：1129 K

摘要

Epidemiological studies have shown that there is a strong correlation between atherosclerosis and ambient air pollution. In this study, we found that motorcycle exhaust particles (MEP) induced adhesion between cells of the human monocytic leukemia cell line (THP-1) and human umbilical vein endothelial cells (HUVECs) in a time-and dose-dependent manner. In addition, MEP treatment induced both mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in HUVECs. The I魏B degradation and p65 nuclear translocation was found in MEP-treated HUVECs, suggested the involvement of nuclear factor-魏B (NF-魏B). MEP-induced VCAM-1 and ICAM-1 protein expression was inhibited by NF-魏B inhibitor BAY 11-7085. Oxidative stress was also involved in the signaling of VCAM-1 and ICAM-1 expression. MEP treatment caused hydrogen peroxide and superoxide formation. Pretreatment with 伪-tocopherol could inhibit MEP-induced reactive oxygen intermediates generation and suppressed MEP-induced I魏B degradation and adhesion molecules expression. Furthermore, the carbon black (CB) nanoparticles with different diameters could induce VCAM-1 and ICAM-1 protein expression; however, polycyclic aromatic hydrocarbons (PAHs) only increased the expression of ICAM-1 but not that of VCAM-1 in HUVECs. In this study, we found that MEPs could induce ICAM-1 and VCAM-1 expression through oxidative stress and NF-魏B activation in HUVECs.