Inhibitory Effect of Ghrelin on Nicotine-induced VCAM-1 Expression in Human Umbilical Vein Endothelial Cells

被引:18
作者
Hu, Cui-Zhu [1 ]
Cao, Yan-Li [2 ]
Huo, Hai-Yang [1 ]
Zhao, Wei-Hua [1 ]
Hu, Jian [1 ]
机构
[1] China Med Univ, Affiliated Hosp 1, Dept Cardiol, Shenyang 110001, Liaoning, Peoples R China
[2] China Med Univ, Affiliated Hosp 1, Dept Endocrinol, Shenyang 110001, Liaoning, Peoples R China
关键词
adhesion molecules; atherosclerosis; endothelial cells; ghrelin; smoking; ACTIVATED PROTEIN-KINASE; NF-KAPPA-B; ADHESION MOLECULE-1; GENE-EXPRESSION; DOWN-REGULATION; INSULIN; ATHEROSCLEROSIS; PROLIFERATION; MONOCYTES; RESPONSES;
D O I
10.1097/FJC.0b013e31819c74dc
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Endothelial dysfunction is thought to be a major cause of vascular injury in smokers. Ghrelin is a recently discovered peptide that plays a modulatory role in atherosclerosis. However, it is unknown how ghrelin regulates nicotine-induced vascular cell adhesion molecule-1 (VCAM-1) expression. We examined nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells pretreated with ghrelin and detected the activity of protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor (NF)-kappa B. Our study showed that ghrelin inhibited nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells in a concentration-dependent and time-dependent way. We also found that ghrelin inhibited nicotine-induced PKC, p38 MAPK, and NF-kappa B activation. The results suggest that ghrelin inhibits nicotine-induced VCAM-1 expression, and PKC, p38 MAPK, and NF-kappa B play active roles in that process. Exogenous ghrelin may provide a possible approach for preventing or reversing atherosclerosis in smokers.
引用
收藏
页码:241 / 245
页数:5
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