Asunto(s)
Enfermedades del Ano/virología , Carcinoma Verrugoso/virología , Condiloma Acuminado/virología , Neoplasias de los Genitales Masculinos/virología , Papillomavirus Humano 6/aislamiento & purificación , Infecciones por Papillomavirus/complicaciones , Escroto , Enfermedades del Ano/patología , Enfermedades del Ano/cirugía , Carcinoma Verrugoso/patología , Carcinoma Verrugoso/cirugía , Condiloma Acuminado/patología , Condiloma Acuminado/cirugía , Neoplasias de los Genitales Masculinos/patología , Neoplasias de los Genitales Masculinos/cirugía , Papillomavirus Humano 11/aislamiento & purificación , Humanos , Masculino , Persona de Mediana Edad , Infecciones por Papillomavirus/patología , Infecciones por Papillomavirus/cirugía , Escroto/virología , Resultado del TratamientoRESUMEN
The human brain is uniquely powerful in its cognitive abilities, yet the hippocampal and neocortical circuits that mediate these complex functions are highly vulnerable during aging. In this study, we analyzed age-related changes in the rat hippocampus by studying newborn (1 month), middle-aged (12 months), and older (24 months) male and female Sprague-Dawley rats. We evaluated neuronal dystrophy, neuron scattering, and granulovacuolar degeneration in the hippocampal area using light microscopy, according to age and gender. We detected significant neuronal dystrophy in the CA1, CA2, and CA3 areas in male rats, and in the CA1, CA3, and CA4 areas in female rats. Degenerative changes, indicated by neuron scattering, were observed in the CA1, CA2, and CA3 areas of male and the CA2 and CA4 areas of female rats. Changes in all areas of the hippocampus were observed with increasing age; these changes included neuronal dystrophy and neuron scattering and did not differ significantly between male and female rats.
Asunto(s)
Envejecimiento , Hipocampo/anatomía & histología , Hipocampo/fisiología , Distrofias Neuroaxonales/fisiopatología , Factores de Edad , Precursor de Proteína beta-Amiloide/metabolismo , Animales , Femenino , Masculino , Degeneración Nerviosa , Distrofias Neuroaxonales/patología , Neuronas/patología , Neuronas/fisiología , Ratas , Ratas Sprague-Dawley , Factores SexualesRESUMEN
In this study, we aimed to investigate the possible protective effect of resveratrol on gentamicin induced nephrotoxicity. Experiments were carried out in male Wistar rats weighing 200-250 g. Gentamicin sulfate (80 mg/kg per day i.p.), resveratrol (10 mg/kg per day i.p.) and gentamicin together with resveratrol were administered for 6 d. The animals were sacrificed 24 h after the last injection. Urine, blood samples and tissue samples were collected from the animals on the seventh day of the treatment before they were sacrificed. Kidneys were collected for histopathological studies and fixed in 10% buffered formalin solution. Tissue samples were stored at -70 degrees C in liquid nitrogen for the determination of glutathione (GSH), glutathione-S-transferase (GST), malondialdehyde (MDA) and catalase (CAT). Glutathione assay was determined by the method of Beutler et al. GST amounts were measured by the method of Habig et al. Catalase activity was tested by Aebi's method and MDA was determined according to Thayer's method. Blood urea level was significantly increased in the gentamicin treated group. The study showed lowered levels of urea and creatinine levels in resveratrol administered groups when compared with gentamicin administered rats, and the difference was statistically significant. It has been determined that resveratrol caused statistically significant decrease in lipid peroxidation and reduced the level of catalase. Histopathological examination showed that resveratrol prevented partly gentamicin induced tubular damage. The results histopathologically demonstrated that resveratrol has a protective effect against gentamicin induced nephrotoxicity, lipid peroxidation and cellular damage in rats.
Asunto(s)
Antibacterianos , Antioxidantes/farmacología , Gentamicinas , Enfermedades Renales/prevención & control , Riñón/efectos de los fármacos , Peroxidación de Lípido/efectos de los fármacos , Estilbenos/farmacología , Animales , Antioxidantes/uso terapéutico , Catalasa/metabolismo , Creatinina/sangre , Glutatión/metabolismo , Glutatión Transferasa/metabolismo , Riñón/metabolismo , Riñón/patología , Enfermedades Renales/sangre , Enfermedades Renales/inducido químicamente , Enfermedades Renales/metabolismo , Enfermedades Renales/patología , Túbulos Renales/efectos de los fármacos , Masculino , Malondialdehído/metabolismo , Potasio/sangre , Ratas , Ratas Wistar , Resveratrol , Sodio/sangre , Estilbenos/uso terapéutico , Urea/sangreRESUMEN
Free radical-mediated injury to lung and pulmonary vasculature is an important mechanism in hypoxia-induced lung damage. In this study, we aimed to investigate the potential protective effects of erdosteine as an antioxidant agent on hypobaric hypoxia-induced pulmonary hypertension. Adult male rats were assigned randomly to three groups. The first group of rats was exposed to hypobaric-hypoxia and the second group was treated with erdosteine (20mg/kg, daily) for 2 weeks, during which time they were in a hypoxic chamber. These groups were compared with normoxic controls. All rats were sacrificed after 2 weeks. The hypoxia-induced increase in right ventricle to left ventricle plus septum weight ratio (from 0.20+/-0.01 to 0.26+/-0.01) was reduced significantly in the erdosteine-treated group (0.23+/-0.01). Malondialdehyde levels were elevated (from 0.33+/-0.11 to 0.59+/-0.02) and total antioxidant status was not changed significantly (from 1.77+/-0.42 to 2.61+/-0.23) by hypoxia. In contrast to the hypoxia-exposed group, malondialdehyde levels were significantly decreased in the erdosteine-treated group (0.37+/-0.02). Total antioxidant status (4.03+/-0.22) was significantly higher in erdosteine-treated rats when compared to non-treated rats. Histopathological examination demonstrated that erdosteine prevented inflammation and protected lung parenchyma and pulmonary endothelium of hypoxia-exposed rats.