Purpose To investigate the protective effect of aminoguanine( AG) on vasodilatation of rat aortic rings injured by high fructose and its mechanism. Methods The isolated thoracic aortic rings of male SD rats were mounted on the organ bath and the tension was recorded isometrically. The effect of AG and fructose on the rings with endothelium intact precontracted by the phenylephrine ( PE, 1 μmol/L), and the vessel relaxation to acetochloriline was recorded with biological signal analytical system,the expression of p-Akt、p-eNOS or p-ERK1/2 in aortic rings was detected by western blot and the content of NO in vessels was analyzed by nitrate reduction method. Results The high fructose inhibited the relaxation to Ach,and AG improve the reaction in a concentration-dependent manner in endothelium-intact rat aorta. The expression of p-eNOS in aortic rings and NO content are also reduced by high fructose,but the expression of p-Akt has no significant difference among groups. Furthermore, the phosphorylation of ERK1/2 increased in arotic rings incubated with high fructose,and AG could inhibited the phosphorylation. Conclusion AG improved endothelium-dependent relaxation injured by high fructose, which probably up-regulated eNOS activity by inhibition of ERK1/2 phosphorylation.%目的 探讨氨基胍对高果糖致大鼠离体胸主动脉环内皮依赖性舒张反应损伤的保护作用及机制.方法 用离体血管环灌流装置,观察不同浓度氨基胍对高果糖引起血管内皮依赖性舒张反应损伤的保护作用；并分析血管壁中NO含量以及eNOS、Akt和ERK1/2蛋白磷酸化的表达.结果 高果糖抑制乙酰胆碱诱导的内皮依赖性舒张,降低血管壁中NO的含量和eNOS活性,并促进ERK1/2磷酸化水平上调,但对Akt磷酸化无显著影响；用氨基胍与高果糖共同孵育后,明显改善高果糖对内皮依赖性舒张反应的损伤并恢复血管壁NO含量和eNOS活性,同时降低ERKl/2磷酸化水平.结论 氨基胍能改善高果糖对离体胸主动脉环内皮依赖舒张反应的损伤作用.其保护机制与抑制ERK1/2磷酸化和恢复eNOS活性有关,而与AKT磷酸化活性无关.
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