Protective effects of enzymatic digest from Ecklonia cava against high glucose-induced oxidative stress in human umbilical vein endothelial cells.
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 carbohydrate, Celluclast.


RESULTS
High glucose treatment induced HUVECs cell death, but ECC, at a concentration of 10 or 100 microg 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.


CONCLUSIONS
These results suggest that ECC is a potential therapeutic agent that will reduce the damage caused by hyperglycaemia-induced oxidative stress associated with diabetes.
Lee
Seung-Hong
SH
School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of South Korea.
Heo
Soo-Jin
SJ
Hwang
Ji-Young
JY
Han
Ji-Sook
JS
Jeon
You-Jin
YJ
D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects*; D004798:Enzymes / Q000378:metabolism; D005947:Glucose / Q000009:adverse effects*; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D000459:Phaeophyceae / Q000737:chemistry* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances; D014471:Umbilical Veins
D000975:Antioxidants; D004798:Enzymes; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D005947:Glucose