6,6′-Bieckol Isolated from Ecklonia cava Protects Oxidative Stress Through Inhibiting Expression of ROS and Proinflammatory Enzymes in High-Glucose-Induced Human Umbilical Vein Endothelial Cells
Hyperglycemia-induced oxidative stress accelerates endothelial cell dysfunctions, which cause various complications of diabetes. The protective effects of 6,6′-bieckol (BEK), one of phlorotannin compound purified from Ecklonia cava against high-glucose-induced oxidative stress was investigated using...
Gespeichert in:
Veröffentlicht in: | Applied biochemistry and biotechnology 2014-09, Vol.174 (2), p.632-643 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Hyperglycemia-induced oxidative stress accelerates endothelial cell dysfunctions, which cause various complications of diabetes. The protective effects of 6,6′-bieckol (BEK), one of phlorotannin compound purified from
Ecklonia 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-κB) 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. |
---|---|
ISSN: | 0273-2289 1559-0291 |
DOI: | 10.1007/s12010-014-1099-4 |