Abstract
Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats Wen-Chao Liu, Liang Wen, Hao Wang, Jiang-Biao Gong, Tian-Xiang Zhan, Yuan-Yuan Meng, Xiao-Feng Yang Department of Neurosurgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China Abstract: In the present study, we evaluated the changes in autophagy after hyperbaric oxygen (HBO) treatment for traumatic brain injury (TBI) and investigated whether autophagy takes part in the neuroprotection after HBO treatment. Male Sprague Dawley rats were assigned to four groups randomly: sham injury, sham injury and HBO, TBI, and TBI and HBO. The HBO rats received HBO treatment for 100 min immediately after injury. Rats were sacrificed at 24 h after the brain injury and the levels of cleaved caspase-3 and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells in the injured cortex were measured to determine cell death. The expression levels of autophagy-associated proteins were measured by immunohistochemistry and Western blotting to assess changes in autophagy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cell density and cleaved caspase-3 expression were increased 24 h after TBI. These increases were suppressed by post-TBI HBO treatment. Immunohistochemistry and Western blotting of autophagy-associated proteins showed that TBI can induce autophagy and that HBO treatment can further upregulate the expression of autophagy makers, as shown by an increase in LC3, ATG-5, and Beclin-1 expression and reduction in P62 expression. In conclusion, HBO treatment can reduce apoptosis and further upregulate autophagy in the injured cortex after brain injury, and the autophagy pathway may take part in the neuroprotection provided by HBO treatment for TBI. Keywords: autophagy, hyperbaric oxygen treatment, traumatic brain injury, apoptosis, neuroprotective effect
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
