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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:519.)
© 2007 American Heart Association, Inc.

Vascular Biology

Anthocyanin Prevents CD40-Activated Proinflammatory Signaling in Endothelial Cells by Regulating Cholesterol Distribution

Min Xia; Wenhua Ling; Huilian Zhu; Qing Wang; Jing Ma; Mengjun Hou; Zhihong Tang; Lan Li; Qinyuan Ye

From the Department of Nutrition, School of Public Health, Sun Yat-Sen University (Northern Campus), Guangzhou, PR China.

Correspondence to Wenhua Ling, MD, PhD, Professor, Dean, Department of Nutrition, School of Public Health, Sun Yat-Sen University (Northern Campus), Guangzhou, Guangdong Province, PR China 510080. E-mail lingwh{at}mail.sysu.edu.cn

Objective— Intracellular tumor necrosis factor receptor-associated factors (TRAFs) translocation to lipid rafts is a key element in CD40-induced signaling. The purpose of this study was to investigate the influence of anthocyanin on CD40-mediated proinflammatory events in human endothelial cells and the underlying possible molecular mechanism.

Methods and Results— Treatment of endothelial cells with anthocyanin prevented from CD40-induced proinflammatory status, measured by production of IL-6, IL-8, and monocyte chemoattractant protein-1 through inhibiting CD40-induced nuclear factor-B (NF-B) activation. TRAF-2 played pivotal role in CD40–NF-B pathway as TRAF-2 small interference RNA (siRNA) diminished CD40-induced NF-B activation and inflammation. TRAF-2 overexpression increased CD40-mediated NF-B activation. Moreover, TRAF-2 almost totally recruited to lipid rafts after stimulation by CD40 ligand and depletion of cholesterol diminished CD40-mediated NF-B activation. Exposure to anthocyanin not only interrupted TRAF-2 recruitment to lipid rafts but also decreased cholesterol content in Triton X-100 insoluble lipid rafts. However, anthocyanin did not influence the interaction between CD40 ligand and CD40 receptor.

Conclusions— Our findings suggest that anthocyanin protects from CD40-induced proinflammatory signaling by preventing TRAF-2 translocation to lipid rafts through regulation of cholesterol distribution, which thereby may represent a mechanism that would explain the anti-inflammatory response of anthocyanin.

Intracellular tumor necrosis factor receptor-associated factors (TRAFs) translocation to lipid rafts is a key element in CD40-induced signaling. The purpose of this study was to investigate the influence of anthocyanin on CD40-mediated proinflammatory events in human endothelial cells and the underlying possible molecular mechanism.

Key Words: arteriosclerosis • cholesterol • endothelium • inflammation

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