Protective effect of diphlorethohydroxycarmalol isolated from Ishige okamurae against high glucose-induced-oxidative stress in human umbilical vein endothelial cells |
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Authors: | Soo-Jin Heo Ji-Young Hwang Jung-In Choi Seung-Hong Lee Pyo-Jam Park Do-Hyung Kang Chulhong Oh Dong-Woo Kim Ji-Sook Han You-Jin Jeon Hak-Ju Kim Il-Whan Choi |
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Institution: | 1. Marine Living Resources Research Department, Korea Ocean Research and Development Institute, Ansan 426-744, Republic of Korea;2. Department of Food Science and Nutrition, Pusan National University, Busan 609-735, Republic of Korea;3. School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea;4. Department of Biotechnology, Konkuk University, Chungju 380-701, Republic of Korea;5. Central Research Center, Natural F&P Co., Ltd., O-Chang, Chungbuk 363-883, Republic of Korea;6. Seojin Biotech Co. Ltd, Maethan 3-dong, Eongtong-gu, Suwon, Gyeonggi-do 443-373, Republic of Korea;g Department of Microbiology and Bio-Marker Research Center for Personalized Therapy, College of Medicine, Inje University, Busan 614-735, Republic of Korea |
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Abstract: | In the present study, the protective effect of diphlorethohydroxycarmalol (DPHC) isolated from Ishige okamurae, a brown algae, on high glucose-induced-oxidative stress was investigated using human umbilical vein endothelial cells (HUVECs). High concentration of glucose (30 mM) treatment induced cytotoxicity whereas DPHC prevented cells from high glucose-induced damage; restoring cell viability was significantly increased. In addition, the lipid peroxidation, intracellular reactive oxygen species (ROS), and nitric oxide (NO) levels induced by high glucose treatment were effectively inhibited by addition of DPHC in a dose-dependent manner. DPHC also suppressed the over-expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins as well as nuclear factor-kappa B (NF-κB) activation induced by high glucose in HUVECs. These finding indicate that DPHC might be used as potential pharmaceutical agent which will reduce the damage caused by high glucose-induced-oxidative stress associated with diabetes. |
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