Bioactive compounds extracted from Ecklonia cava by using enzymatic hydrolysis protects high glucose-induced damage in INS-1 pancreatic β-cells.
Pancreatic β-cells are very sensitive to oxidative stress and this might play an important role in β-cell death in diabetes. In the present study, we investigated whether the brown alga Ecklonia cava has protective effects against high glucose-induced damage in INS-1 pancreatic β-cells. For that purpose, we prepared an enzymatic hydrolysate from E. cava (EHE) by using the carbohydrase, Celluclast. High-glucose (30 mM) treatment induced glucotoxicity, whereas EHE prevented cells from high glucose-induced damage then restoring cell viability was significantly increased. Furthermore, lipid peroxidation, intracellular reactive oxygen species (ROS) and nitric oxide (NO) were overproduced as the result of the treatment by high glucose; however, these lipid peroxidation, ROS and NO generations were effectively inhibited by addition of EHE in a dose-dependent manner. Moreover, EHE treatment increased activities of antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) in high glucose pretreated INS-1 pancreatic β-cells. EHE slightly reduced the expression of pro-apoptotic protein Bax induced by high glucose but increased the expression of Bcl-2, an anti-apoptotic protein. These findings indicate that EHE might be used as potential nutraceutical agent which will protect the glucotoxicity caused by hyperglycemia-induced oxidative stress associated with diabetes.
Department of Marine Life Science, Jeju National University, Jeju 690-756, South Korea.
Seung-Hong
SH
Lee
Mi-Hwa
MH
Park
Sun-Joo
SJ
Park
Jaeil
J
Kim
Yong-Tae
YT
Kim
Myung-Cheol
MC
Oh
Yoonhwa
Y
Jeong
Misook
M
Kim
Ji-Sook
JS
Han
You-Jin
YJ
Jeon
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D001688:Biological Products / Q000302:isolation & purification* / Q000494:pharmacology*; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D019610:Cytoprotection / Q000187:drug effects*; D057075:Enzyme Assays; D005947:Glucose / Q000633:toxicity*; D006026:Glycoside Hydrolases / Q000378:metabolism*; D006868:Hydrolysis / Q000187:drug effects; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D009569:Nitric Oxide / Q000096:biosynthesis; D000459:Phaeophyceae / Q000737:chemistry*; D059808:Polyphenols / Q000494:pharmacology; D011134:Polysaccharides / Q000494:pharmacology; D020011:Protective Agents / Q000494:pharmacology; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013194:Staining and Labeling; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D000975:Antioxidants; D001688:Biological Products; D059808:Polyphenols; D011134:Polysaccharides; D020011:Protective Agents; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D051028:bcl-2-Associated X Protein; D009569:Nitric Oxide; D006026:Glycoside Hydrolases; C019822:carbohydrase; D005947:Glucose