Phlorotannin protects oxidative stress through inhibiting expression of ROS and proinflammatory enzymes in high-glucose-induced HUVECs

DC Field Value Language
dc.contributor.author 허수진 -
dc.contributor.author 예보람 -
dc.contributor.author 장지이 -
dc.contributor.author 김민선 -
dc.contributor.author 이승홍 -
dc.contributor.author 전유진 -
dc.date.accessioned 2020-07-16T02:53:51Z -
dc.date.available 2020-07-16T02:53:51Z -
dc.date.created 2020-02-11 -
dc.date.issued 2014-10-27 -
dc.identifier.uri https://sciwatch.kiost.ac.kr/handle/2020.kiost/25899 -
dc.description.abstract 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. 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. -
dc.description.uri 2 -
dc.language English -
dc.publisher 한국해양바이오학회 -
dc.relation.isPartOf The 10th KSMB Annual Meeting & Symposium -
dc.title Phlorotannin protects oxidative stress through inhibiting expression of ROS and proinflammatory enzymes in high-glucose-induced HUVECs -
dc.type Conference -
dc.citation.conferencePlace KO -
dc.citation.endPage 93 -
dc.citation.startPage 93 -
dc.citation.title The 10th KSMB Annual Meeting & Symposium -
dc.contributor.alternativeName 허수진 -
dc.contributor.alternativeName 예보람 -
dc.contributor.alternativeName 장지이 -
dc.contributor.alternativeName 김민선 -
dc.identifier.bibliographicCitation The 10th KSMB Annual Meeting & Symposium, pp.93 -
dc.description.journalClass 2 -
Appears in Collections:
Jeju Research Institute > Jeju Marine Research Center > 2. Conference Papers
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