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1.
Behav Neurol ; 2021: 6651492, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-33833828

RESUMEN

Symptoms of depressive disorders such as anhedonia and despair can be a product of an aberrant adaptation to stress conditions. Chronic unpredictable stress model (CUS) can generate an increase in the activity of the hypothalamic-pituitary-adrenal axis (HPA) and induce a reduction of neurotrophin signaling and the proliferation of neural progenitors in the adult dentate gyrus, together with increased oxidative stress. Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH). We aimed to evaluate the effects of FAAH inhibitor, URB597, on depressive-like behavior and neural proliferation of mice subjected to a model of CUS. URB597 was administered intraperitoneally at a dose of 0.2 mg/kg for 14 days after CUS. Depressive-like behaviors, anhedonia, and despair were evaluated in the splash and forced swimming tests, respectively. Alterations at the HPA axis level were analyzed using the relative weight of adrenal glands and serum corticosterone levels. Oxidative stress and brain-derived neurotrophic factor (BDNF) were also evaluated. Fluorescence immunohistochemistry tests were performed for the immunoreactivity of BrdU and Sox2 colabeling for comparison of neural precursors. The administration of URB597 was able to reverse the depressive-like behavior generated in mice after the model. Likewise, other physiological responses associated with CUS were reduced in the treated group, among them, increase in the relative weight of the adrenal glands, increased oxidative stress, and decreased BDNF and number of neural precursors. Most of these auspicious responses to enzyme inhibitor administration were blocked by employing a cannabinoid receptor antagonist. In conclusion, the chronic inhibition of FAAH generated an antidepressant effect, promoting neural progenitor proliferation and BDNF expression, while reducing adrenal gland weight and oxidative stress in mice under the CUS model.


Asunto(s)
Sistema Hipotálamo-Hipofisario , Sistema Hipófiso-Suprarrenal , Amidohidrolasas , Animales , Proliferación Celular , Corticosterona , Giro Dentado , Modelos Animales de Enfermedad , Ratones , Estrés Psicológico/tratamiento farmacológico
3.
Neurosci Lett ; 321(1-2): 100-4, 2002 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-11872266

RESUMEN

During cerebral ischemia-reperfusion, the enhanced production of oxygen-derived free radicals contributes to neuronal death. The antioxidants alpha-lipoic acid and vitamin E have shown synergistic effects against lipid peroxidation by oxidant radicals in several pathological conditions. A thromboembolic stroke model in rats was used to analyze the effects of this mixture under two oral treatments: intensive and prophylactic. Neurological functions, glial reactivity and neuronal remodeling were assessed after experimental infarction. Neurological recovery was only found in the prophylactic group, and both antioxidant schemes produced down-regulation of astrocytic and microglial reactivity, as well as higher neuronal remodeling in the penumbra area, as compared with controls. The beneficial effects of this antioxidant mixture suggest that it may be valuable for the treatment of cerebral ischemia in humans.


Asunto(s)
Encéfalo/efectos de los fármacos , Gliosis/tratamiento farmacológico , Hipoxia-Isquemia Encefálica/tratamiento farmacológico , Plasticidad Neuronal/efectos de los fármacos , Recuperación de la Función/efectos de los fármacos , Ácido Tióctico/farmacología , Vitamina E/farmacología , Animales , Astrocitos/citología , Astrocitos/metabolismo , Encéfalo/patología , Encéfalo/fisiopatología , Modelos Animales de Enfermedad , Depuradores de Radicales Libres/farmacología , Proteína GAP-43/metabolismo , Proteína Ácida Fibrilar de la Glía/metabolismo , Gliosis/patología , Gliosis/fisiopatología , Hipoxia-Isquemia Encefálica/patología , Hipoxia-Isquemia Encefálica/fisiopatología , Masculino , Microglía/citología , Microglía/metabolismo , Degeneración Nerviosa/tratamiento farmacológico , Degeneración Nerviosa/patología , Degeneración Nerviosa/fisiopatología , Plasticidad Neuronal/fisiología , Estrés Oxidativo/efectos de los fármacos , Estrés Oxidativo/fisiología , Ratas , Ratas Wistar , Recuperación de la Función/fisiología , Sinaptofisina/metabolismo , Tromboembolia/tratamiento farmacológico , Tromboembolia/patología , Tromboembolia/fisiopatología
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