Hangaishi M, Taguchi J, Miyata T, Ikari Y, Togo M, Hashimoto Y, Watanabe T, Kimura S, Kurokawa K, Ohno M
Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Biochem Biophys Res Commun. 1998 Jul 20;248(2):285-92. doi: 10.1006/bbrc.1998.8945.
Advanced glyco-oxidation end products (AGEs) generate oxygen free radicals that potentiate the development of atherosclerosis. Thus, AGEs may potentiate the aggregation of human platelets through oxidative stress. AGE-bovine serum albumin (BSA) and AGE-poly-L-lysine were evaluated for aggregation of human platelets. Superoxide in platelet-rich plasma (PRP) was measured using lucigenin-derived chemiluminescence. The platelet aggregation induced by ADP or U46619 was potentiated by preincubation with AGE-BSA, by 40% and by 59%, P < .05, respectively, vs BSA. Aggregation was increased by AGEs in a dose-dependent manner. The production of superoxide was significantly greater in PRP incubated with AGE-BSA vs BSA. The other Maillard reaction products, such as Amadori-, pentosidine-, and carboxymethyl lysine (CML)-BSA had no effect. Superoxide dismutase or indomethacin abolished the enhancing effect of AGEs on the platelet aggregation. AGEs potentiate platelet aggregation possibly with superoxide anions and prostanoids. AGE-induced potentiation of platelet aggregation may be involved in the development of atherosclerosis.
晚期糖基化终末产物（AGEs）会产生氧自由基，从而促进动脉粥样硬化的发展。因此，AGEs可能通过氧化应激增强人血小板的聚集。对AGE-牛血清白蛋白（BSA）和AGE-聚-L-赖氨酸诱导人血小板聚集的情况进行了评估。使用光泽精化学发光法测定富血小板血浆（PRP）中的超氧化物。与BSA相比，预先与AGE-BSA孵育可使ADP或U46619诱导的血小板聚集分别增强40%和59%，P <.05。AGEs以剂量依赖的方式增加聚集。与BSA相比，与AGE-BSA孵育的PRP中超氧化物的产生显著增加。其他美拉德反应产物，如阿马多里产物、戊糖苷和羧甲基赖氨酸（CML）-BSA则没有影响。超氧化物歧化酶或吲哚美辛可消除AGEs对血小板聚集的增强作用。AGEs可能通过超氧阴离子和前列腺素增强血小板聚集。AGEs诱导的血小板聚集增强可能与动脉粥样硬化的发展有关。
