Cytoprotective Role of Astaxanthin against Glycated Protein/Iron Chelate-induced Toxicity in Human Umbilical Vein Endothelial Cells

被引:47
作者
Nishigaki, Ikuo [1 ]
Rajendran, Peramaiyan [1 ]
Venugopal, Ramachandran [1 ]
Ekambaram, Gnapathy [1 ]
Sakthisekaran, Dhanapal [2 ]
Nishigaki, Yutaka [3 ]
机构
[1] NPO Int Lab Biochem, Nakagawa Ku, Nagoya, Aichi 4540926, Japan
[2] Univ Madras, Dept Med Biochem, Madras 600113, Tamil Nadu, India
[3] Tokyo Metropolitan Inst Gerontol, Itabashi Ku, Tokyo 1790015, Japan
基金
英国工程与自然科学研究理事会;
关键词
glycated protein; iron; HUVEC; astaxanthin; antioxidant enzymes; OXIDATIVE STRESS; DIABETES-MELLITUS; FREE-RADICALS; GLUCOSE; DAMAGE; CAROTENOIDS; MODEL; MEMBRANE; PEROXIDE; PROTECTS;
D O I
10.1002/ptr.2867
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Astaxanthin (ASX), a red carotenoid pigment with no pro-vitamin A activity, is a biological antioxidant that occurs naturally in a wide variety of plants, algae and seafoods. This study investigated whether ASX could inhibit glycated protein/iron chelate-induced toxicity in human umbilical-vein endothelial cells (HUVEC) by interfering with ROS generation in these cells. Glycated fetal bovine serum (GFBS) was prepared by incubating fetal bovine serum (FBS) with high-concentration glucose. Stimulation of cultured HUVECs with 50 mM 1 mL of GFBS significantly enhanced lipid peroxidation and decreased antioxidant enzyme activities and levels of phase II enzymes. However, preincubation of the cultures with ASX resulted in a marked decrease in the level of lipid peroxide (LPO) and an increase in the levels of antioxidant enzymes in an ASX concentration-dependent manner. These results demonstrate that ASX could inhibit LPO formation and enhance the antioxidant enzyme status in GFBS/iron chelate-exposed endothelial cells by suppressing ROS generation, thereby limiting the effects of the AGE-RAGE interaction. The results indicate that ASX could have a beneficial role against glycated protein/iron chelate-induced toxicity by preventing lipid and protein oxidation and increasing the activity of antioxidant enzymes. Copyright (C) 2009 John Wiley & Sons, Ltd.
引用
收藏
页码:54 / 59
页数:6
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