Effects of prolonged ingestion of epigallocatechin gallate on diabetes type 1-induced vascular modifications in the erectile tissue of rats

• Published in: International journal of impotence research 2016-07, Vol.28 (4), p.133-138
• Main Authors: Lombo, C, Morgado, C, Tavares, I, Neves, D
• Format: Article
• Language: English
• Subjects: 13; 13/51; 692/499; 692/699/75; 692/699/75/2099; 82; 82/80; Animals; Antioxidants; Biological products; Blood circulation disorders; Care and treatment; Catechin; Catechin - analogs & derivatives; Catechin - therapeutic use; Complications and side effects; Diabetes; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Type 1 - complications; Diabetes Mellitus, Type 1 - metabolism; Diabetes Mellitus, Type 1 - pathology; Diabetes therapy; Diabetic Angiopathies - drug therapy; Diabetic Angiopathies - metabolism; Diabetic Angiopathies - pathology; Endothelium; Erectile dysfunction; Health aspects; Impotence; Male; Medicine; Medicine & Public Health; Muscle, Smooth - drug effects; Muscle, Smooth - metabolism; Muscle, Smooth - pathology; original-article; Penis - drug effects; Penis - metabolism; Penis - pathology; Rats; Rats, Wistar; Reproductive Medicine; Risk factors; Rodents; rology; Sexual disorders; Smooth muscle; Type 1 diabetes; Urology; Vascular endothelial growth factor; Vascular Endothelial Growth Factor A - metabolism; Vascular Endothelial Growth Factor Receptor-1 - metabolism; Vascular Endothelial Growth Factor Receptor-2 - metabolism
• ISSN: 0955-9930; 1476-5489
• DOI: 10.1038/ijir.2016.19

Diabetes Mellitus type 1 is a metabolic disease that predisposes to erectile dysfunction, partly owing to structural and molecular changes in the corpus cavernosum (CC) vessels. The aim of this study was to determine the effects of early treatment with the antioxidant epigallocatechin gallate (EGCG) in cavernous diabetes-induced vascular modifications. Diabetes was induced in two groups of young Wistar rats; one group was treated with EGCG for 10 weeks. A reduction in smooth muscle content was observed in the CC of diabetic rats, which was significantly attenuated with EGCG consumption. No differences were observed among groups, neither in the expression of VEGF assayed by western blotting nor in the immunofluorescent labeling of vascular endothelial growth factor (VEGF) and its receptors (VEGFR1 and VEGFR2). VEGFR2 was restricted to the endothelium, whereas VEGF and VEGFR1 co-localized in the smooth muscle layer. With regard to the Angiopoietin/Tie-2 system, no quantitative differences in Angiopoietin 1 were observed among the experimental groups. Ang1 localization was restricted to the smooth muscle layer, and receptor Tie2 and Angiopoietin 2 were both expressed in the endothelium. In brief, our results suggest that EGCG consumption prevented diabetes-induced loss of cavernous smooth muscle but does not affect vascular growth factor expression in young rats.