RESUMO
AIM: Genetic absence epilepsy rats from Strasbourg (GAERS) provide a model of absence epilepsy. Although excessive GABA mediation within the thalamo-cortico-thalamic circuit has been shown to play a role in absence epilepsy, neuronal networks of hippocampus have recently received attention. Glutamic acid decarboxylase (GAD) was previously shown to be increased after convulsive seizures in the mossy fiber terminals (MFTs) of hippocampus. The aim of the present study was to investigate whether the change in the level of this enzyme in convulsive seizures is also observed in rats having genetic absence epilepsy. MATERIAL AND METHODS: Hippocampal CA3 and dentate regions were processed for transmission electron microscopic evaluations. Thin sections were incubated with anti-GAD65/67 antibody. The NIH Image Analysis program was used for the quantitative analysis. RESULTS: It was observed that GAD65/67 immunoreactivity was positive in CA3 and dentate gyrus MFTs of both groups and the difference in the density of immunolabeling between the groups was not statistically significant. CONCLUSION: The present study demonstrated that GABA synthesizing enzyme, GAD, is found in MFTs of Wistar and GAERS hippocampus and this enzyme does not show an increase in these terminals in absence epilepsy, in contrast to convulsive seizures.
Assuntos
Epilepsia Tipo Ausência/enzimologia , Glutamato Descarboxilase/metabolismo , Hipocampo/enzimologia , Fibras Musgosas Hipocampais/enzimologia , Ácido gama-Aminobutírico/biossíntese , Animais , Região CA3 Hipocampal/enzimologia , Região CA3 Hipocampal/ultraestrutura , Giro Denteado/enzimologia , Giro Denteado/ultraestrutura , Modelos Animais de Doenças , Epilepsia Tipo Ausência/genética , Epilepsia Tipo Ausência/fisiopatologia , Predisposição Genética para Doença/genética , Glutamato Descarboxilase/genética , Hipocampo/fisiopatologia , Hipocampo/ultraestrutura , Masculino , Microscopia Imunoeletrônica/métodos , Fibras Musgosas Hipocampais/ultraestrutura , Inibição Neural/genética , Terminações Pré-Sinápticas/enzimologia , Terminações Pré-Sinápticas/ultraestrutura , Ratos , Ratos Mutantes , Ratos Wistar , Transmissão Sináptica/genéticaRESUMO
BACKGROUND: Urinary tract infection (UTI) may cause inflammation of the renal parenchyma and may lead to impairment in renal function and scar formation. Oxidant injury and reactive oxygen species (ROS) have been found responsible in the pathogenesis of UTI. The neurohypophyseal hormone oxytocin (OT) facilitates wound healing and is involved in the modulation of immune and inflammatory processes. We investigated the possible therapeutic effects of OT against Escherichia coli induced pyelonephritis in rats both in the acute and chronic setting. METHODS: Twenty-four Wistar rats were injected 0.1 ml solution containing E. coli ATCC 25922 10(10) colony forming units/ml into left renal medullae. Six rats were designed as sham group and were given 0.1 ml 0.9% NaCl. Pyelonephritic rats were treated with either saline or OT immediately after surgery and at daily intervals. Half of the pyelonephritic rats were decapitated at the 24th hour of E. coli infection, and the rest were followed for 7 days. Renal function tests (urea, creatinine), systemic inflammation markers [lactate dehydrogenase (LDH) and tumor necrosis factor alpha (TNF-alpha)] and renal tissue malondialdehyde (MDA) as an end product of lipid peroxidation, glutathione (GSH) as an antioxidant parameter and myeloperoxidase (MPO) as an indirect index of neutrophil infiltration were studied. RESULTS: Blood urea, creatinine, and TNF-alpha levels were increased, renal tissue MDA and MPO levels were elevated and GSH levels were decreased in both of the pyelonephritic (acute and chronic) rats. All of these parameters and elevation of LDH at the late phase were all reversed to normal levels by OT treatment. CONCLUSION: OT alleviates oxidant renal injury in pyelonephritic rats by its anti-oxidant actions and by preventing free radical damaging cascades that involves excessive infiltration of neutrophils.
Assuntos
Antioxidantes/uso terapêutico , Rim/efeitos dos fármacos , Neutrófilos/efeitos dos fármacos , Estresse Oxidativo , Ocitocina/uso terapêutico , Pielonefrite/tratamento farmacológico , Animais , Antioxidantes/farmacologia , Colágeno/metabolismo , Creatinina/sangue , Creatinina/metabolismo , Glutationa/metabolismo , Rim/citologia , Rim/patologia , Testes de Função Renal , L-Lactato Desidrogenase/sangue , L-Lactato Desidrogenase/metabolismo , Masculino , Malondialdeído/metabolismo , Neutrófilos/citologia , Neutrófilos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ocitocina/farmacologia , Pielonefrite/complicações , Pielonefrite/metabolismo , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa , Ureia/sangue , Ureia/metabolismoRESUMO
Alendronate (ALD) causes serious gastrointestinal adverse effects. The aim of this study was to investigate whether taurine (TAU), a semi-essential amino acid and an antioxidant, improves the alendronate-induced gastric injury. Rats were administered 20 mg/kg ALD by gavage for 4 days, either alone or following treatment with TAU (50 mg/kg, i.p.). On the last day of treatment, following drug administration, pylorus ligation was performed and 2 h later, rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined. Chronic oral administration of ALD induced significant gastric damage, increasing lipid peroxidation, MPO activity and collagen content, as well as decreasing tissue GSH levels. Treatment with TAU prevented the damage and also the changes in biochemical parameters. Findings of the present study suggest that ALD induces oxidative gastric damage by a local irritant effect, and that TAU ameliorates this damage by its antioxidant and/or membrane-stabilizing effects.
