Marine Living Resources Research Department, Korea Ocean Research and Development Institute, Ansan, Republic of Korea.
Food Chem Toxicol. 2010 Jun;48(6):1448-54. doi: 10.1016/j.fct.2010.02.025. Epub 2010 Feb 20.
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-kappaB) 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.
在本研究中，我们研究了来自 Ishige okamurae 的二苯并呋喃二羟基卡玛醇（DPHC）对高糖诱导的氧化应激的保护作用，Ishige okamurae 是一种褐藻。高浓度葡萄糖（30mM）处理会诱导细胞毒性，而 DPHC 可防止细胞受到高糖诱导的损伤；细胞活力明显恢复。此外，DPHC 还可抑制高糖诱导的脂质过氧化、细胞内活性氧（ROS）和一氧化氮（NO）水平的产生，并呈剂量依赖性。DPHC 还可抑制高糖诱导的人脐静脉内皮细胞（HUVECs）中诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）蛋白的过度表达以及核因子-κB（NF-κB）的激活。这些发现表明，DPHC 可作为一种潜在的药物，减少与糖尿病相关的高糖诱导的氧化应激引起的损伤。
