2-3-diaminophenazine and Diabetic-Angiopathies

2-3-diaminophenazine has been researched along with Diabetic-Angiopathies* in 2 studies

Other Studies

2 other study(ies) available for 2-3-diaminophenazine and Diabetic-Angiopathies

ArticleYear
Effects of advanced glycation end-product inhibition and cross-link breakage in diabetic rats.
    Metabolism: clinical and experimental, 2000, Volume: 49, Issue:8

    The accelerated formation of advanced glycation end-products (AGEs) due to elevated glycemia has repeatedly been reported as a central pathogenic factor in the development of diabetic microvascular complications. The effects of a novel inhibitor of AGE formation, NNC39-0028 (2,3-diaminophenazine), and a breaker of already formed AGE cross-links, N-phenacylthiazolium bromide (PTB), were investigated in streptozotocin-diabetic female Wistar rats. Diabetes for 24 weeks resulted in decreased tail collagen pepsin solubility, reflecting the formation of AGE cross-linking. Collagen solubility was significantly ameliorated by treatment with NNC39-0028, whereas PTB had no effect. Increased urinary albumin excretion (UAE) in diabetic rats was observed in serial measurements throughout the study period, and was not reduced by any treatment. Vascular dysfunction in the eye, measured as increased clearance of 125I-albumin, was induced by diabetes. NNC39-0028 did not affect this abnormality. This study demonstrated a pharmacological inhibition of collagen solubility alterations in diabetic rats without affecting diabetes-induced pathophysiology such as the increase in UAE or albumin clearance. Treatment with PTB, a specific breaker of AGE cross-links, had no effects in this study.

    Topics: Albuminuria; Animals; Collagen; Diabetes Mellitus, Experimental; Diabetic Angiopathies; Drinking; Eye; Female; Glycation End Products, Advanced; Kidney; Organ Size; Phenazines; Radiopharmaceuticals; Rats; Rats, Wistar; Serum Albumin; Serum Albumin, Radio-Iodinated; Solubility; Tail; Tendons; Thiazoles; Weight Gain

2000
A novel inhibitor of advanced glycation end-product formation inhibits mesenteric vascular hypertrophy in experimental diabetes.
    Diabetologia, 1999, Volume: 42, Issue:4

    Previous studies in our laboratory have shown that the vascular changes in diabetes include hypertrophy of the mesenteric vasculature and that this process can be attenuated by the inhibition of advanced glycation with aminoguanidine. Since aminoguanidine can also act as an inhibitor of nitric oxide synthase, the effect of a novel inhibitor of advanced glycation end-products, formation that does not inhibit nitric oxide synthase, known as 2,3 diaminophenazine (2,3 DAP) was evaluated.. Initially, in vitro assessment of the ability of 2,3 diaminophenazine to inhibit formation of advanced glycation products was performed. Subsequently, in vivo studies evaluating 2,3 diaminophenazine and aminoguanidine were carried out. Animals were followed for 3 weeks after induction of diabetes and randomised to no treatment, aminoguanidine or 2,3 diaminophenazine. Mesenteric vessels were weighed and advanced glycation end-products were measured by radioimmunoassay in vessel and kidney homogenates. In addition, these products were assessed in mesenteric vessels by immunohistochemistry.. When compared with control animals, diabetes was associated with an increase in mesenteric vascular weight. Treatment of diabetic rats with aminoguanidine or 2,3 diaminophenazine resulted in attenuation of vascular hypertrophy. Both aminoguanidine and 2,3 diaminophenazine reduced the formation of advanced glycation end-products as measured by radioimmunoassay and as assessed immunohistochemically in these vessels. This reduction was also observed in the kidney.. These data support the concept that the effects of aminoguanidine in reducing diabetes associated vascular hypertrophy are via inhibition of advanced glycation end-products dependent pathways.

    Topics: Animals; Diabetes Mellitus, Experimental; Diabetic Angiopathies; Enzyme Induction; Glycation End Products, Advanced; Hypertrophy; Male; Mesenteric Arteries; Mesenteric Veins; Mice; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Phenazines; Rabbits; Radioimmunoassay; Rats; Rats, Sprague-Dawley

1999
chemdatabank.com