Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway

Background: Given that the therapeutic effect of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) has been debated for a long time, it is necessary to clarify the mechanism underlying the effect of HBO on acute TBI. Methods: This study investigated the effect of HBO therapy on neuronal apoptosis induced by acute TBI using the mouse model of TBI. The number of apoptotic cells and expression of apoptosis-associated factors (including caspase 3, pAkt/Akt, pGSK3 beta/GSK3 beta, and beta-catenin) in pericontusional cortices of mice exposed to sham, TBI, and TBI + HBO treatment were measured and analyzed using TUNEL assay, quantitative reverse-transcription PCR, and Western blot. Results: Results showed that acute TBI increased the number of apoptotic neurons and mRNA expression and activated caspase 3 protein. With regard to proteins, acute TBI also resulted in decreased levels of pAkt/Akt, pGSK3 beta/GSK3 beta, and beta-catenin, which facilitates neuronal apoptosis. This study shows that HBO therapy reversed these changes of pAkt/Akt, pGSK3 beta/GSK3 beta, and beta-catenin induced by acute TBI and attenuated the apoptotic process in the pericontusional cortex. Conclusion: This study demonstrates the beneficial effect of HBO therapy on neuronal apoptosis caused by acute TBI. Furthermore, the mechanism underlying the therapeutic effect of HBO on acute TBI partly involves the Akt/GSK3 beta/beta-catenin pathway.