title: Dieckol isolated from Ecklonia cava protects against high-glucose induced damage to rat insulinoma cells by reducing oxidative stress and apoptosis.
abstract: Pancreatic β cells are very sensitive to oxidative stress and this might play an important role in β cell death with diabetes. The protective effect of dieckol, one of the phlorotannin polyphenol compounds purified from Ecklonia cava (E. cava), against high glucose-induced oxidative stress was investigated by using rat insulinoma cells. A high-glucose (30 mM) treatment induced the death of rat insulinoma cells, but dieckol, at a concentration 17.5 or 70 µM, significantly inhibited the high-glucose induced glucotoxicity. Treatment with dieckol also dose-dependently reduced thiobarbituric acid reactive substances (TBARS), the generation of intracellular reactive oxygen species (ROS), and the nitric oxide level increased by a high glucose concentration. In addition, the dieckol treatment increased the activities of antioxidative enzymes including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) in high glucose-pretreated rat insulinoma cells. Dieckol protected rat insulinoma cells damage under high glucose conditions. These effects were mediated by suppressing apoptosis and were associated with increased anti-apoptotic Bcl-2 expression, and reduced pro-apoptotic cleaved caspase-3 expression. These findings indicate that dieckol might be useful as a potential pharmaceutical agent to protect against the glucotoxicity caused by hyperglycemia-induced oxidative stress associated with diabetes.
authors.affiliation: Department of Marine Life Science, Jeju National University, Jeju 690-756, Korea.
authors.forename: Seung-Hong
authors.initials: SH
authors.lastname: Lee
authors.forename: Mi-Hwa
authors.initials: MH
authors.lastname: Park
authors.forename: Sung-Myung
authors.initials: SM
authors.lastname: Kang
authors.forename: Seok-Chun
authors.initials: SC
authors.lastname: Ko
authors.forename: Min-Cheol
authors.initials: MC
authors.lastname: Kang
authors.forename: Seungmok
authors.initials: S
authors.lastname: Cho
authors.forename: Pyo-Jam
authors.initials: PJ
authors.lastname: Park
authors.forename: Byong-Tae
authors.initials: BT
authors.lastname: Jeon
authors.forename: Se-Kwon
authors.initials: SK
authors.lastname: Kim
authors.forename: Ji-Sook
authors.initials: JS
authors.lastname: Han
authors.forename: You-Jin
authors.initials: YJ
authors.lastname: Jeon
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000302:isolation & purification / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001572:Benzofurans / Q000302:isolation & purification / Q000494:pharmacology*; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002374:Catalase / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015870:Gene Expression / Q000187:drug effects; D005947:Glucose / Q000009:adverse effects; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D007340:Insulinoma / Q000378:metabolism / Q000473:pathology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D018384:Oxidative Stress / Q000187:drug effects; D000459:Phaeophyceae / Q000737:chemistry*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000975:Antioxidants; D001572:Benzofurans; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; C503840:dieckol; D009569:Nitric Oxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D053148:Caspase 3; D005947:Glucose