糖基化终产物对巨噬细胞产生一氧化氮及其合酶活性的影响  

Effect of advanced glycosylation end products on level of nitric oxide and activity of nitric oxide synthase in cultured macrophages

作　　者：严金川[1] 黄晓明[2] 刘乃丰[2] 

机构地区：[1]镇江市第四人民医院心内科,江苏镇江212001 [2]南京铁道医学院,江苏南京210009

出　　处：《中国病理生理杂志》2000年第9期839-841,共3页Chinese Journal of Pathophysiology

摘　　要：目的 :探讨糖基化终产物 (AGEs)对巨噬细胞一氧化氮通路的影响及其机制。方法 :应用一氧化氮 (NO)及一氧化氮合酶 (NOS)试剂盒测定巨噬细胞产生NO和NOS活性。结果 :巨噬细胞产生NO含量及NOS活性随AGEs作用时间延长明显减少 ,并且随AGEs的浓度、糖化程度加重、葡萄糖修饰浓度增加 ,巨噬细胞产生NO含量及NOS活性呈减弱趋势 ,VitE明显增加巨噬细胞产生NO含量以及NOS活性。结论 :AGEs通过抑制巨噬细胞NOS活性而抑制其产生NO ,VitE对巨噬细胞具有保护作用 ,能减轻AGEs的损害作用 。AIM:To study the mechanism and effect of advanced glycosylation end products (AGEs) on NO pathway in cultured macrophages.METHODS:The level of NO and NOS activity were measured by NO and NOS kits in cultured macrophages. RESULTS:The results showed that AGEs induced decreases in NO level and NOS activity in a time and dose-related manner in interleukin-1 (IL-1)-stimulated macrophages. VitE can significantly inhibited effects of AGEs on IL-1-stimulated macrophages. CONCLUSION:AGEs can decrease NO production via inhibiting NOS activity in IL-1-stimulated macrophages. VitE can protect the cells from AGEs injury. It is an important theoretical basis for preventing chronic complication in diabetes mellitus.

关 键 词：糖基化终产物 巨噬细胞 一氧化氮 IL-1 NOS 

分 类 号：R587.2[医药卫生—内分泌]