ABSTRACT
A escala mundial, la isquemia cerebral constituye una de las principales causas de muerte, por lo que los modelos animales de isquemia cerebral son extensamente usados tanto en el estudio de la pato-fisiología del fenómeno isquémico; como en la evaluación de agentes terapéuticos con posible efecto protector o regenerador. Los objetivos de este estudio fueron examinar la presencia de daño neuronal en diferentes áreas cerebrales como consecuencia del evento isquémico; así como evaluar consecuencias de este proceder sobre los procesos de memoria-aprendizaje. Los grupos de estudios incluyeron un grupo experimental de animales isquémicos, 30 ratas a las que se les ocluyó ambas arterias carótidas comunes, y un grupo control. Fue evaluada la expresión de genes isquémicos e inflamatorios por técnicas de qPCR 24 horas post lesión, la morfología del tejido cerebral en áreas de corteza, estriado e hipocampo, siete días post lesión y los procesos de memoria y aprendizaje, 12 días post lesión. Los estudios morfológicos evidenciaron que el proceder induce la muerte de poblaciones celulares en corteza, estriado e hipocampo; la isquemia modificó la expresión los genes gfap, ho-1, il-6, il-17 e ifn-γ, lo cual puede ser utilizado como un marcador de proceso isquémico temprano. Adicionalmente, el daño isquémico causó un deterioro en la memoria espacial. Esta caracterización nos permite contar con un modelo experimental donde desarrollar futuros estudios sobre la patofisiología de los eventos isquémicos y la evaluación de estrategias terapéuticas.
Cerebral ischemia is a major cause of death, for this reason animal models of cerebral ischemia are widely used to study both the pathophysiology of ischemic phenomenon and the evaluation of possible therapeutic agents with protective or regenerative properties. The objectives of this study were to examine the presence of neuronal damage in different brain areas following the ischemic event, and assess consequences of such activities on the processes of memory and learning. The study group included an experimental group ischemic animals (30 rats with permanent bilateral occlusion of the carotids), and a control group. Was evaluated gene expression and inflammatory ischemic by qPCR techniques 24h post injury, brain tissue morphology in areas of cortex, striatum and hippocampus seven days post injury and processes of memory and learning, 12 days post injury. The morphological studies showed that the procedure induces death of cell populations in cortex, striatum and hippocampus, ischemia modified gfap gene expression and ho, il-6, il-17 and ifn-γ, which can be used as a marker of early ischemic process. Additionally, the ischemic injury caused spatial memory decline. This characterization gives us an experimental model to develop future studies on the pathophysiology of ischemic events and assessing therapeutic strategies.
ABSTRACT
Aims: The etiology of autism spectrum disorders (ASD) remains elusive, but oxidative stress has been suggested to play a pathological role. The understanding of the potential role of oxidative stress in the etiopathogenesis of autism would be very useful for earlier clinical, therapeutic or preventive strategies. Sample: To evaluate the redox status, we quantified the activity of the antioxidant enzyme catalase (CAT), glutathione concentration (GSH) and markers of damage to biomolecules, malonyldialdehyde (MDA) and 8–hydroxy-2deoxyguanosine (8OHdG) in peripheral blood samples. Place and Duration of Study: Sample: Department of Neuropediatrics and Technology Science Division. International Center for Neurological Restoration (CIREN), Havana, Cuba. May 2011- June 2012. Methodology: We included 45 children with autism (36 males and 9 females, age-range from 3 to 11 years). 42 children of the same age were selected as a control group. The diagnosis of autism was made based on the criteria of autistic disorders as defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM IV) (American Psychiatric Association, 1994). Results: The total GSH content in autistic patients was significantly lower compared with the control group (0.24 ± 0.162 vs. 0.94 ± 0.115, respectively, p ≤ 0.001). Higher serum CAT, MDA and 8OHdG levels were found in children with autism compared with controls (CAT, 2.836 ± 0.479 vs. 0.689 ± 0.157, p ≤ 0.001; MDA 8.6 ± 0.5 vs. 1.76 ± 0.33 p ≤ 0.001, and 8OHdG 13.134 ± 1.33 vs.1.46 ± 0.326, p ≤ 0.001). Conclusion: The present study supports the notion that oxidative stress is associated with autism, but additional researches are needed to investigate how it may contribute to autistic pathophysiology and these studies are currently in progress.