Leonurine protects against tumor necrosis factor-伪-mediated inflammation in human umbilical vein endothelial cells

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• 作者：Xinhua Liu^a ; ¹ ; Lilong Pan^a ; ¹ ; Xianli Wang^a ; Qihai Gong^a ; Yi Zhun Zhu^a ; ^b ; ^{zhuyz@fudan.edu.cn}
• 关键词：Leonurine ; Atherosclerosis ; Inflammation ; Human umbilical vein endothelial cells ; Adhesion molecules ; Cyclooxygenase-2 ; Reactive oxygen species
• 刊名：Atherosclerosis
• 出版年：2012
• 期刊代码：28_00219150
• 类别：med
• 出版时间：May, 2012
• 卷：222
• 期：1
• 页码：34-42
• 文件大小：1496 K

摘要

Objective

Leonurine, a bioactive alkaloid compound in Herba leonuri, has various pharmacological activities, including antioxidant and anti-apoptotic capacities. This study was conducted to test the hypothesis that leonurine was able to attenuate tumor necrosis factor (TNF)-伪-induced human umbilical vein endothelial cells (HUVEC) activation and the underlying molecular mechanisms.

Methods

Mitogen-activated protein kinases (MAPK) activation, nuclear factor-魏B (NF-魏B) activation, and inflammatory mediators expression were detected by Western blot or enzyme-liked immunosorbent assay, intracellular reactive oxygen species (ROS) and NF-魏B p65 translocation were measured by immunofluorescence, endothelial cell-monocyte interaction was detected by microscope.

Results

Leonurine inhibited U937 cells adhesion to TNF-伪-activated HUVEC in a concentration dependent manner. Treatment with leonurine blocked TNF-伪-induced mRNA and protein expression of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1), cyclooxygenase-2, and monocyte chemoattractant protein-1 in endothelial cells. In addition, leonurine attenuated TNF-伪-induced intracellular ROS production in HUVEC. Furthermore, leonurine also suppressed the TNF-伪-activated p38 phosphorylation and I魏B伪 degradation. Subsequently, reduced NF-魏B p65 phosphorylation, nuclear translocation, and DNA-binding activity were also observed.

Conclusions

Our results demonstrated for the first time that the anti-inflammatory properties of leonurine in endothelial cells, at least in part, through suppression of NF-魏B activation, which may have a potential therapeutic use for inflammatory vascular diseases.