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Effects of Eicosapentaenoic Acid on the Cytoprotection Through Nrf2-Mediated Heme Oxygenase-1 in Human Endothelial Cells.

Abstract
Consumption of omega-3 polyunsaturated fatty acid, particularly eicosapentaenoic acid (EPA), is associated with a significant reduction in the risk of developing cardiovascular disease. The aim of this study was to investigate whether heme oxygenase-1 (HO-1) induction contributes to the cytoprotective effects of EPA in endothelial cells threatened with oxidative damage. In this study, we investigated the effect of EPA on the induction of HO-1 by NF-E2-related factor 2 (Nrf2) in human umbilical vein endothelial cells. In cells treated with low concentrations of EPA (10-25 μM), HO-1 expression increased in a time- and concentration-dependent manner. Additionally, EPA treatment increased Nrf2 nuclear translocation and antioxidant response element activity, leading to the upregulation of HO-1 expression. Furthermore, treatment with EPA reduced hydrogen peroxide (H(2)O(2))-induced cell death. The reduction in cell death was reversed by treatment with zinc protoporphyrin, an inhibitor of HO-1, indicating that HO-1 contributed to the protective effect of EPA. These data suggest that EPA protects against H(2)O(2)-induced oxidative stress in endothelial cells by activating Nrf2 and inducting HO-1 expression.
AuthorsSeung Eun Lee, Gun-Dong Kim, Hana Yang, Gun Woo Son, Hye Rim Park, Jeong-Je Cho, Hyun-Jong Ahn, Cheung-Seog Park, Yong Seek Park
JournalJournal of cardiovascular pharmacology (J Cardiovasc Pharmacol) Vol. 66 Issue 1 Pg. 108-17 (Jul 2015) ISSN: 1533-4023 [Electronic] United States
PMID25815672 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Eicosapentaenoic Acid
  • Heme Oxygenase-1
Topics
  • Cytoprotection (drug effects, physiology)
  • Dose-Response Relationship, Drug
  • Eicosapentaenoic Acid (pharmacology)
  • Heme Oxygenase-1 (physiology)
  • Human Umbilical Vein Endothelial Cells (drug effects, physiology)
  • Humans
  • NF-E2-Related Factor 2 (physiology)

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