Cystatin C has a dual role in post-traumatic brain injury recovery.

Cathepsin B is one of the major lysosomal cysteine proteases involved in neuronal protein catabolism. This cathepsin is released after traumatic injury and increases neuronal death; however, release of cystatin C, a cathepsin inhibitor, appears to be a self-protective brain response. Here we describe the effect of cystatin C intracerebroventricular administration in rats prior to inducing a traumatic brain injury. We observed that cystatin C injection caused a dual response in post-traumatic brain injury recovery: higher doses (350 fmoles) increased bleeding and mortality, whereas lower doses (3.5 to 35 fmoles) decreased bleeding, neuronal damage and mortality. We also analyzed the expression of cathepsin B and cystatin C in the brains of control rats and of rats after a traumatic brain injury. Cathepsin B was detected in the brain stem, cerebellum, hippocampus and cerebral cortex of control rats. Cystatin C was localized to the choroid plexus, brain stem and cerebellum of control rats. Twenty-four hours after traumatic brain injury, we observed changes in both the expression and localization of both proteins in the cerebral cortex, hippocampus and brain stem. An early increase and intralysosomal expression of cystatin C after brain injury was associated with reduced neuronal damage.

Sleep deprivation has a neuroprotective role in a traumatic brain injury of the rat.

During the process of a brain injury, responses to produce damage and cell death are activated, but self-protective responses that attempt to maintain the integrity and functionality of the brain are also activated. We have previously reported that the recovery from a traumatic brain injury (TBI) is better in rats if it occurs during the dark phase of the diurnal cycle when rats are in the waking period. This suggests that wakefulness causes a neuroprotective role in this type of injury. Here we report that 24h of total sleep deprivation after a TBI reduces the morphological damage and enhances the recovery of the rats, as seen on a neurobiological scale.

Neuroprotección y traumatismo craneoencefálico / Neuroprotection and traumatic brain injury

Durante un proceso de lesión cerebral, por ejemplo en un traumatismo craneoencefálico, se activan respuestas que inducen daño cerebral o muerte celular; sin embargo, también se inducen respuestas de protección que intentan mantener la integridad y funcionalidad del cerebro; esto se conoce como neuroprotección. Efectivamente, posterior a un TCE, se desencadenan mecanismos que traen como consecuencia liberación de neurotransmisores excitadores tales como el glutamato, lo que provoca una entrada masiva de Ca²+ en las neuronas, activación de proteasas, lipasas, sintasa de óxido nítrico, endonucleasas, producción de radicales libres y potencialmente necrosis o apoptosis. Aunque hay reportes de sustancias neuro o cerebroprotectoras desde hace más de 50 años, es al final de la década de los ochenta del siglo pasado cuando comienza a aparecer un gran número de publicaciones tratando de entender los mecanismos neuroprotectores desencadenados por un insulto al cerebro. En este trabajo revisamos brevemente el concepto, la epidemiologia y los diversos agentes que se han utilizado para disminuir el daño causado por un traumatismo craneoencefálico.

During a process of brain injury, e.g. head injury, responses to induce brain damage and / or cell death are activated, but also protective responses that attempt to maintain the integrity and functionality of the brain are induced. This is known as neuroprotection. Indeed a head injury triggers mechanisms that result in release of excitatory neurotransmitters such as glutamate, which causes an influx of Ca²+ into neurons, activation of proteases, lipases, nitric oxide synthase, endonucleases, free radicals production and potentially necrosis and / or apoptosis. Although the brain or neuroprotective substances research has more than 50 years, is at the end of the decade of 80's of last century when it began to appear a large number of publications trying to understand the neuroprotective mechanisms triggered by an insult to the brain. In this paper we briefly review the concept, epidemiology and strategies that have been used to minimize the damage caused by brain injury.