Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway
Authors He H, Li X, He Y
Received 12 August 2018
Accepted for publication 27 October 2018
Published 25 January 2019 Volume 2019:15 Pages 369—374
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Yuping Ning
Hui He,1 Xiufang Li,2 Yuling He1
1Department of Emergency, Zhuji People’s Hospital of Zhejiang Province, Zhuji, Zhejiang, China; 2Department of Pathology, Zhuji People’s Hospital of Zhejiang Province, Zhuji, Zhejiang, China
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, pGSK3β/GSK3β, and β-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, pGSK3β/GSK3β, and β-catenin, which facilitates neuronal apoptosis. This study shows that HBO therapy reversed these changes of pAkt/Akt, pGSK3β/GSK3β, and β-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/GSK3β/β-catenin pathway.
Keywords: hyperbaric oxygen, TBI, apoptosis, Akt, GSK3β, β-catenin
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