Effects of Eicosapentaenoic Acid on the Cytoprotection Through Nrf2-Mediated Heme Oxygenase-1 in Human Endothelial Cells. Issue 1 (July 2015)

• Record Type: Journal Article
• Authors: Lee, Seung Eun; Kim, Gun-Dong; Yang, Hana; Son, Gun Woo; Park, Hye Rim; Cho, Jeong-Je; Ahn, Hyun-Jong; Park, Cheung-Seog; Park, Yong Seek
• Is Part Of: Journal of cardiovascular pharmacology. Volume 66:Issue 1(2015)
• Publication Date: 2015-07
• Subjects: EPA -- HO-1 -- Nrf2 -- endothelial cells -- oxidative stress; Cardiovascular Diseases -- drug therapy -- Periodicals; Cardiovascular System -- drug effects -- Periodicals; Cardiovascular pharmacology -- Periodicals; Cardiovascular agents -- Periodicals; Cardiovascular agents; Cardiovascular pharmacology; Periodicals; 615.7105
• DOI: 10.1097/FJC.0000000000000251
• Languages: English
• ISSNs: 0160-2446

Abstract

Abstract : 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 (H2 O2 )-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 H2 O2 -induced oxidative stress in endothelial cells by activating Nrf2 and inducting HO-1 expression.