Introduction: Cardiovascular diseases, including cardiomyopathies associated with endothelial dysfunction and impaired protein glycation, are the predominant cause of mortality in diabetes mellitus. This article presents data on the identification of functional and structural changes occurring during the development of diabetic cardiomyopathy and investigates the cardioprotective effects of the anti-glycating agents – the azolo-triazine derivative AB-19 and aminoguanidine. Materials and Methods: Diabetic cardiomyopathy was modeled using streptozotocin 45 mg/kg I.V. on 60 male Sprague-Dawley rats. Aminoguanidine was investigated at the dose of 50 mg/kg and compound AB-19 – 20 mg/kg once daily. Observations were conducted over a period of 12 weeks. Blood glucose levels and glycated hemoglobin concentration were monitored. Upon completion of the diabetic cardiomyopathy induction period, the following were studied: endothelioprotective properties, cardiac contractile activity, solubility of tail tendon collagen and morphological examinations of the heart and myocardial blood vessels. Results: The oral administration of AB-19 (20 mg/kg) and aminoguanidine (50 mg/kg) to animals with experimental diabetes mellitus resulted in a 17% reduction in blood HbA1c levels compared to that in the diabetic control rats. This treatment also limited the increase in AGEs in the blood by 51% and 39%, improved the solubility of collagen by 42% and 51%, respectively, restored endothelium-dependent vascular reactivity, and attenuated manifestations of left ventricular diastolic dysfunction associated with myocardial hypertrophy and fibrosis in diabetic animals. These findings were morphologically corroborated: animals treated with AB-19 and aminoguanidine exhibited a reduction in perivascular connective tissue, a decrease in collagen fibers in the myocardium, and a lower expression of AGEs and RAGE in IHC analysis using primary antibodies against AGEs and RAGE compared to the diabetic control group. Conclusion: Compound AB-19 (20 mg/kg once daily) attenuates functional and structural manifestations of diabetic cardiomyopathy.
Gurova et al. (2026) studied this question.