Effects of aminoguanidine treatment on endothelial nitric oxide synthase expression and nitric oxide levels in streptozotocin induced diabetic rats

Abstract

Objective: Formation of advanced glycation end products (AGE) in Diabetes Mellitus contribute to endothelial dysfunction by permanent modifications of proteins and decrease NO concentration which regulate vascular tonicity and thus endothelial functions. We investigated the effects of AGE inhibitor aminoguanidine (AG) treatment on endothelial nitric oxide synthase (eNOS) expression and NO levels in streptozotocin induced diabetic rats. Material and method: 38 male Sprague-Dawley rats were separated into 4 groups. Group 1 was healthy controls without any intervention (HC group). Group 2 received AG in drinking water (HC+AG group). Third and fourth groups received 65 mg/kg streptozotocin intraperitoneally to induce diabetes. Group 3 was followed without further intervention (DM group). Group 4 received aminoguanidine in drinking water (DM+AG group). After 12 weeks, glucose, HbA 1c , NO levels an eNOS expressions were determined. Results: NO levels were significantly lower in DM and HC+AG groups compared to HC group. There was no significant difference between the NO levels of DM and DM+AG groups. eNOS protein levels in heart tissues were significantly lower in DM group than the HC group. eNOS levels were significantly higher in DM+AG than DM group. There was no significant difference in eNOS levels in kidney tissues among the groups. Conclusion: Decreased NO levels in DM group was consistent with the literature. eNOS expression in heart tissues were decreased in DM group, their concentration were increased with AG therapy. Further studies are needed to elaboate the effects of AG in tissues and the side effects observed in some studies.