Inhibitory effect of Malvidin on TNF-α-induced inflammatory response in endothelial cells.

Abstract

Vascular inflammatory responses are key mediators of endothelial dysfunction that leads to various pathologies in many diseases including atherosclerosis and cancer. The purpose of the study was to investigate the effects and molecular mechanisms of Malvidin, a natural pigment with strong antioxidant activity, on regulating inflammatory response in endothelial cells. Our results showed that tumor necrosis factor-alpha (TNF-α) significantly increased the protein or mRNA levels of monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), whereas pretreatment with Malvidin inhibited TNF-α-induced increases of MCP-1, ICAM-1, and VCAM-1 production in a concentration-dependent manner. In addition, Malvidin could inhibit degradation of IκBα and the nuclear translocation of p65, which suggesting the anti-inflammation mechanism of Malvidin by the nuclear factor kappa B (NF-κB) pathway. These results indicate the potential role of Malvidin in preventing chronic inflammation in many diseases.

• Authors: Wu-Yang Huang, Jian Wang, Ya-Mei Liu, Qi-Sheng Zheng, Chun-Yang Li
• Journal: European journal of pharmacology (Eur J Pharmacol) Vol. 723 Pg. 67-72 (Jan 15 2014) ISSN: 1879-0712 [Electronic] Netherlands
• PMID: 24333549 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2013 Published by Elsevier B.V.

Chemical References

• Anthocyanins
• Anti-Inflammatory Agents
• Antioxidants
• CCL2 protein, human
• Chemokine CCL2
• I-kappa B Proteins
• NF-kappa B
• NFKBIA protein, human
• RNA, Messenger
• Tumor Necrosis Factor-alpha
• Vascular Cell Adhesion Molecule-1
• malvidin
• Intercellular Adhesion Molecule-1
• NF-KappaB Inhibitor alpha

Topics

• Anthocyanins (pharmacology)
• Anti-Inflammatory Agents (pharmacology)
• Antioxidants (pharmacology)
• Cells, Cultured
• Chemokine CCL2 (genetics, metabolism)
• Human Umbilical Vein Endothelial Cells (drug effects, metabolism)
• Humans
• I-kappa B Proteins (metabolism)
• Intercellular Adhesion Molecule-1 (genetics, metabolism)
• NF-KappaB Inhibitor alpha
• NF-kappa B (metabolism)
• RNA, Messenger (metabolism)
• Tumor Necrosis Factor-alpha (antagonists & inhibitors)
• Vascular Cell Adhesion Molecule-1 (metabolism)