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胃饥饿素对尼古丁诱导的人脐静脉内皮细胞中血管细胞黏附分子-1表达的抑制作用。

Inhibitory effect of ghrelin on nicotine-induced VCAM-1 expression in human umbilical vein endothelial cells.

作者信息

Hu Cui-Zhu, Cao Yan-Li, Huo Hai-Yang, Zhao Wei-Hua, Hu Jian

机构信息

Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, China.

出版信息

J Cardiovasc Pharmacol. 2009 Mar;53(3):241-5. doi: 10.1097/FJC.0b013e31819c74dc.

Abstract

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)-kappaB. 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-kappaB activation. The results suggest that ghrelin inhibits nicotine-induced VCAM-1 expression, and PKC, p38 MAPK, and NF-kappaB play active roles in that process. Exogenous ghrelin may provide a possible approach for preventing or reversing atherosclerosis in smokers.

摘要

内皮功能障碍被认为是吸烟者血管损伤的主要原因。胃饥饿素是最近发现的一种肽,在动脉粥样硬化中起调节作用。然而,尚不清楚胃饥饿素如何调节尼古丁诱导的血管细胞黏附分子-1(VCAM-1)的表达。我们检测了用胃饥饿素预处理的人脐静脉内皮细胞中尼古丁诱导的VCAM-1表达,并检测了蛋白激酶C(PKC)、p38丝裂原活化蛋白激酶(p38 MAPK)和核因子(NF)-κB的活性。我们的研究表明,胃饥饿素以浓度和时间依赖性方式抑制人脐静脉内皮细胞中尼古丁诱导的VCAM-1表达。我们还发现,胃饥饿素抑制尼古丁诱导的PKC、p38 MAPK和NF-κB活化。结果表明,胃饥饿素抑制尼古丁诱导的VCAM-1表达,PKC、p38 MAPK和NF-κB在该过程中起积极作用。外源性胃饥饿素可能为预防或逆转吸烟者的动脉粥样硬化提供一种可能的方法。

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