AGEs诱发体外大鼠心脏微血管内皮细胞iNOS表达

目的观察体外原代培养心脏微血管内皮细胞内一氧化氮(NO)生成与诱导型一氧化氮合酶(iNOS)表达的变化及相关性。方法采用不同浓度牛血清白蛋白糖基化终末产物(BSA-AGEs)(50~200 mg/L)分别作用于心脏微血管内皮细胞(0~24 h),检测NO生成,免疫组化及Western blot检测iNOS表达。结果随着AGEs浓度增加及作用时间的延长,心脏微血管内皮细胞中NO生成增多,iNOS表达也增多(P<0.05)。结论BSA-AGEs可以诱发心脏微血管内皮细胞产生毒性NO,从而引发以微血管内皮功能障碍为特征的糖尿病性心肌病。

AGEs induces the expression of INOS in cultured cardiac microvascular endothelial cells of rat

Objective To observe the effect of the advanced glycation end products(AGEs)on the iNOS expression in cultured cardiac microvascular endothelial cells.Methods Cultured the cardiac microvascular endothelial cells in vitro.After AGEs of the different dose(50～200 mg/L)and different times(0～24 h)played the role on the cells,we determined the NO generation and iNOS protein expression of all groups.Results NO generation and iNOS protein expression increased with the AGEs-dose increasing and treatment time.The results were significantly different.Conclusion These results demonstrate that AGEs may induce iNOS to produce toxic NO in cardiac microvascular endothelial cells,then the diabetic cardiomyopathy occures.