4.7 Article

Protective effect of diphlorethohydroxycarmalol isolated from Ishige okamurae against high glucose-induced-oxidative stress in human umbilical vein endothelial cells

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 48, Issue 6, Pages 1448-1454

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2010.02.025

Keywords

Diphlorethohydorxycarmalol; Diabetes; Oxidative stress; High glucose; HUVECs

Funding

  1. Ministry of Land, Transport and Maritime Affairs, Republic of Korea
  2. Korea Institute of Marine Science & Technology Promotion (KIMST) [20046002] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  3. Ministry for Food, Agriculture, Forestry & Fisheries (MAFRA), Republic of Korea [F20814808H230000100] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  4. National Research Foundation of Korea [핵06B2605] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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In the present study, the protective effect of diphlorethohydroxycarmalol (DPHC) isolated from Ishige okamurae, a brown algae, on high glucose-induced-oxidative stress was investigated using human umbilical vein endothelial cells (HUVECs). High concentration of glucose (30 mM) treatment induced cytotoxicity whereas DPHC prevented cells from high glucose-induced damage: restoring cell viability was significantly increased. In addition, the lipid peroxidation, intracellular reactive oxygen species (ROS), and nitric oxide (NO) levels induced by high glucose treatment were effectively inhibited by addition of DPHC in a dose-dependent manner. DPHC also suppressed the over-expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins as well as nuclear factor-kappa B (NF-kappa B) activation induced by high glucose in HUVECs. These finding indicate that DPHC might be used as potential pharmaceutical agent which will reduce the damage caused by high glucose-induced-oxidative stress associated with diabetes. (C) 2010 Elsevier Ltd. All rights reserved.

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