| Objective:1.To establish the spinal cord injury model in rats.2.To observe theexpression and duration of autophagy and apoptosis after spinal cord injury (SCI) in rats.3.To research the changes of autophagy and apoptosis in rats after SCI treated by hyperbaricoxygen therapy.Methods:Fifty-four Sprague Dawley (SD) rats, weighing250±30g, were used forthe experimental procedure. They were randomly divided into sham operationgroup(n=6),spinal cord injury group(n=24), and hyperbaric oxygen group(n=24). Thespinal cord injury group and the hyperbaric oxygen group were randomly divided into6h,1d,3d,7d groups after injury.There were six rats in every group. In the sham group,only a laminectomy was performed without contusion. In SCI group and hyperbaricoxygen group,laminectomies at T9were performed, followed by impactor contusion of thespinal cord. The hyperbaric oxygen group rats were given Hyperbaric oxygen management,100minutes per every time, once per day for totally five days. The change of locomotorscores after SCI was evaluated with Basso-Beattie-Bresnahan (BBB) scores system. Atevery time point, we used the Transmission Electron Microscope (TEM) to observe theautophagosome. Western blot were used to detect the changes of LC3and Caspase-3inevey time point after SCI.Results:1. Compared to the SCI group, the BBB scores in hyperbaric oxygen groupwere higher and the differences were statistically significant at7days (P<0.05).2. Spinalcord injury was shown under the transmission electron microscope (TEM). In the shamoperation group, the neurons of nuclear membrane integrity, karyotype ws regular,cytochondriome form of normal distribution in cytoplasm and no autophagosome appeared,the quantity of lysosome did not increase; In the SCI group,the swollen cytochondriomews predominant,vacuolization,the quantity of lysosome ws Increased, karyotype wsirregular mostly, and the formation of numerous autophagosome were observed.3.The expression of LC3and Caspase-3in spinal cord increased at6hours after injury, at3days after injury the expression reached peak, and then decreased at7days. Theexpression levels of LC3and Caspase-3in the SCI group and hyperbaric oxygen groupwere higher (P<0.05) compared to the sham operation group in every time point. Thelevels of LC3and Caspase-3in the hyperbaric oxygen group were significantly lower thanthe SCI group at the same time points (P<0.05).Conclusions:1. Autophagy and apoptosis were clearly activated after spinal cordinjury in rats. Autophagy and apoptosis may play a role in neuronal death following spinalcord trauma.2. The same time course of changes in the expression of autophagy andapoptosis existed in the damaged spinal cord tissue.3. Hyperbaric oxygen might be one ofthe possible mechanism of therapy spinal cord injury by decreasing the expression ofautophagy and apoptosis. |