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Protective effects of enzymatic digest from Ecklonia cava against high glucose‐induced oxidative stress in human umbilical vein endothelial cells
Author(s) -
Lee SeungHong,
Heo SooJin,
Hwang JiYoung,
Han JiSook,
Jeon YouJin
Publication year - 2009
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.3833
Subject(s) - oxidative stress , superoxide dismutase , tbars , umbilical vein , antioxidant , reactive oxygen species , catalase , chemistry , nitric oxide , human umbilical vein endothelial cell , lipid peroxidation , biochemistry , glutathione peroxidase , glutathione , pharmacology , enzyme , biology , organic chemistry , in vitro
BACKGROUND: Antioxidants can prevent pathological damage caused by hyperglycaemia‐induced oxidative stress associated with diabetes. In the present study, we investigated whether the brown alga Ecklonia cava has protective effects against high glucose‐induced oxidative stress in Human umbilical vein endothelial cells (HUVECs). For that purpose, we prepared an enzymatic digest from E. cava (ECC) by using the carbohydrase, Celluclast. RESULTS: High glucose treatment induced HUVECs cell death, but ECC, at a concentration of 10 or 100 µg mL −1 , significantly inhibited the high glucose‐induced cytotoxicity. Furthermore, treatment with ECC dose‐dependently decreased thiobarbituric acid reactive substances (TBARS), intracellular generation of reactive oxygen species, and the nitric oxide level increased by high glucose. In addition, ECC treatment increased activities of antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase in high‐glucose pretreated HUVECs. High glucose levels induced the overexpression of inducible nitric oxide synthase, cyclooxygenase‐2 and nuclear factor‐kappa B proteins in HUVECs, but ECC treatment reduced the overexpression of these proteins. CONCLUSION: These results suggest that ECC is a potential therapeutic agent that will reduce the damage caused by hyperglycaemia‐induced oxidative stress associated with diabetes. Copyright © 2009 Society of Chemical Industry