Protective Effect of 6,6’-bieckol Isolated from Ecklonia cava on High Glucose-induced Oxidative Stress in Human Umbilical Vein Endothelial Cells

Abstract

Hyperglycemia-induced oxidative stress accelerate endothelial cell dysfunctions, which cause various complications of diabetes. The protective effects of 6,6’-bieckol (BEK), one of phlorotannin polyphenol compound purified from Ecklonia cava (E. cava) against high glucose-induced oxidative stress was investigated using Human Umbilical Vein Endothelial Cells (HUVECs), which is susceptible to oxidative stress. High glucose (30 mM) treatment induced HUVECs cell death, but BEK, at concentration 10 or 50 μg/ml, significantly inhibited the high glucose-induced cytotoxicity. Furthermore, treatment with BEK dose-dependently decreased thiobarbituric acid reactive substances (TBARS), intracellular reactive oxygen species (ROS) generation and nitric oxide level increased by high glucose. In addition, high glucose levels induced the overexpressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-kB) proteins in HUVECs, but BEK treatment reduced the overexpressions of these proteins. These findings indicate that BEK is a potential therapeutic agent that will prevent diabetic endothelial dysfunction and related complications.va (E. cava) against high glucose-induced oxidative stress was investigated using Human Umbilical Vein Endothelial Cells (HUVECs), which is susceptible to oxidative stress. High glucose (30 mM) treatment induced HUVECs cell death, but BEK, at concentration 10 or 50 μg/ml, significantly inhibited the high glucose-induced cytotoxicity. Furthermore, treatment with BEK dose-dependently decreased thiobarbituric acid reactive substances (TBARS), intracellular reactive oxygen species (ROS) generation and nitric oxide level increased by high glucose. In addition, high glucose levels induced the overexpressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-kB) proteins in HUVECs, but BEK treatment reduced the overexpressions of these proteins. These findings indicate that BEK is a potential therapeutic agent that will prevent diabetic endothelial dysfunction and related complications.