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The binding of advanced glycation endproducts (AGEs) to a cell-surface receptor for AGEs (RAGE) induces the formation of reactive oxygen species (ROS), which have been causally implicated in the pathogenesis of diabetic vascular complications. Pomegranate fruit extract (PFE) contains, a naturally occurring polyphenolic compound reported to possess potent radical-scavenging and antioxidant properties and to display significant cardiovascular protective action. In this study, we investigated whether PFE could inhibit glycated protein-iron chelate-induced toxicity by interfering with ROS generation in human umbilical-vein endothelial cells (HUVEC). 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 PFE resulted in a marked decrease in the level of lipid peroxide (LPO) and increase in the levels of antioxidant enzymes in a PFE concentration-dependent manner. These results demonstrate that PFE could inhibit LPO 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. Hence, PFE may have therapeutic potential in the prevention and treatment of vascular complications in diabetic patients.