Experiment Research Of Hyperbaric Oxygen On Autophagy Changes In Cerebral Cortex After Brain Explosive Injury In Rats

Background Brain explosive injuries are common trauma type in daily life and modern warfare, also is currently the focus of domestic and foreign military medical research content. The brain neurons of edema, degeneration, necrosis and a series of changes after brain explosive injuries, making complex mechanism of brain injury. Autophagy is a highly conserved celluar degradation pathway, the intracellular macromolecules, such as long-life of unwanted proteins, organelles,etc, were transported to the lysosomes, and degraded into small molecules with biological activity. These small molecules were re-used and maintenanced of cell homeostasis process. In recent years, autophagy was found high expression in the brain injury, may be related to the role of neuron self-protection after brain injury. Hyperbaric oxygen is a non-invasive treatment of brain injury adjuvant approach, and the effect is positive, but the specific mechanism remains unclear. In this paper we establish rat brain explosive injury model. Then we study the changes of autophagy after brain injury and hyperbaric oxygen treatment, and the effect of hyperbaric oxygen therapy on cerebral cortex cell autophagy and apoptosis.Objective (1) To establish the brain explosive injury model in rats; (2) To research of autophagy changes in cerebral cortex after brain explosive injury in rats; (3) To research the effect of hyperbaric oxygen on the changes of autophagy and apoptosis in cerebral cortex after brain explosive injury in rats. Method (1) 600mg TNT electric detonator were exploded over the brain of rats at 8cm,10cm,12cm vertical dimension respectively, the brain hemorrhages were observed by MRI 24 hours after injury. Pathomorphological changes were detected by light microscopy and electron microscopy at 6h,24h,3d,7d after injury. To select the appropriate distance from the explosion, and establish a stable animal model. (2) 600mg TNT electric detonators were exploded over the brain of rats at 12cm distance, RT-PCR and Western blotting were used to detect the changes of Beclin-1 expression in cerebral cortex at 6,24hours,3,7days after injury. (3) 600mg TNT electric detonators were exploded'over the brain of rats at 12cm distance, HBO group rats were given HBO management after explosive injury 3h,22h and the same time every days.RT-PCR and Western blotting were used to detect the changes of Beclin-1 and Caspase-3 in cerebral cortex at 6h,24h,3d,7d.Result (1) 8cm group of rats were almost dead after injuried,10cm group of rats lived longer but no more than 7 days,12cm group of rats all lived more than 7 days. The rats MRI display hemorrhage and contusion, Pathomorphological differences were edema with cortex, meninges, periventricular, neuron body, mitochondria at 24 hours after injury. (2) The expression of Beclin-1 in cerebral cortex increased at 6 hours after injury, at 3 days after injury the expression reached peak, and then decreased at 7days. (3) The expression of Beclin-1 and Caspase-3 in explosive group and HBO group were obviously higher than control group, the Beclin-1 and Caspase-3 in HBO group were lower than explosive group.Conclusion (1) The rat brain explosive injury model with stability and reliability induced by 600mg TNT electric detonator and 12cm distance. (2) The expression of Beclin-1 in the cerebral cortex presents ridge after brain explosive injury, suggesting that autophagy goes high after brain explosive injury, might have responses to stress of neuron injury after brain explosive. (3) Hyperbaric oxygen might be one of the possible mechanism of therapy brain injury by decreasing the autophagy and apoptosis.