Alterações histopatológicas e morfométricas renais e hepáticas em ratos wistar diabéticos, submetidos à dieta hiperlipídica e tratados com metformina, pentoxifilina e melatonina

Detalhes bibliográficos
Ano de defesa: 2017
Autor(a) principal: MACÊDO, Simone Regina Barros de lattes
Orientador(a): SILVA JUNIOR, Valdemiro Amaro da
Banca de defesa: MAIA, Carina Scanoni, OLIVEIRA, Andrea Alice da Fonseca, OLIVEIRA, Fabiana Felix de, ROSSITER, Ana Katharyne Fagundes Ferreira
Tipo de documento: Tese
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal Rural de Pernambuco
Programa de Pós-Graduação: Programa de Pós-Graduação em Biociência Animal
Departamento: Departamento de Morfologia e Fisiologia Animal
País: Brasil
Palavras-chave em Português:
Área do conhecimento CNPq:
Link de acesso: http://www.tede2.ufrpe.br:8080/tede2/handle/tede2/7210
Resumo: The objective of this study was to evaluate the histopathological and morphometric changes in renal and hepatic patients in diabetic Wistar rats submitted to the hyperlipidic diet and treated with metformin, pentoxifylline and melatonin. For the experiments were performed 25 male Wistar rats, 30 days old, kept under animal conditions in the Department of Morphology and Physiology of the Federal Rural University of Pernambuco. These animals were randomly distributed in five groups of animals and fed a hyperlipid diet and experimentally induced to diabetes: (GD) diabetic control group (GMP) treated with metformin (500 mg/kg) and melatonin (5 mg/kg), treated with metformin (GMP) treated with metformin and metformin (100 mg/kg) Pentoxifylline and melatonin. At the end of the experimental period, the animals were anesthetized and perfused, and the kidneys and liver were collected for qualitative and quantitative analysis of the lesions and blood serum for the determination of urea, creatinine, ALT, AST, ALP and GGT. With respect to histopathological lesions, the most frequent in the kidneys were membranous glomerulonephritis, proliferative glomerulonephritis, membranoproliferative glomerulonephritis, glomerular atrophy, contorted tube hydropsy, tube deformed with cellular debris, necrosis and congestion. The most frequent histopathological lesions in the liver were microsesteatosis, macroesteatosis, hepatocyte hypertrophy, narrowing of sinusoidal capillaries, coagulation necrosis, central lobular vein congestion, hepatic parenchyma congestion, hepatocyte cord atrophy, and dilatation of Sinusoidal capillaries. As for histomorphometry there was no difference in the percentage of necrotic hepatocytes, mononuclear hepatocytes, binucleated hepatocytes, blood vessels and bile ducts, Kupffer cells. Regarding the percentage of sinusoidal capillaries, the group treated with metformin associated with melatonin presented statistically higher value than the other groups. Serum urea concentrations were not statistically different between the treated groups and the control group. However, the mean values of the treated animals remained above normal for species. Diabetic animals submitted and treated with metformin + pentoxifylline and the association of these with melatonin provided a tendency to reduce serum urea levels in relation to untreated diabetic animals. No statistical difference was found between groups either. The creatinine values in the groups treated with metformin + melatonin and the association between metformin + pentoxifylline + melanin had a statistically significant reduction of 62% and 67%, respectively, in relation to the untreated diabetic group. It is concluded that pentoxifylline potentiates the reduction of the glycemic levels resulting from the administration of metformin. However, it is not able to reduce the glomerular and hepatic lesions due to diabetes and the administration of a hyperlipidic diet. Metformin associated with melatonin or in combination with pentoxifylline and melatonin protects the renal parenchyma from histopathological lesions and reduces serum creatinine levels, in addition to influencing the reduction of serum ALT levels and damage compatible with non-alcoholic fatty liver disease in Diabetic animals submitted to the hyperlipidic diet.