Abstract

Objective To investigate the expressions of neurite outgrowth inhibitor (Nogo), myelin-associated glycoprotein (MAG) and Nogo receptor-1 (NgR1), and neuro-protective effect of N-Butylphthalide (NBP) in rat brain tissues following acute CO poisoning. Methods Sixty Sprague-Dawley rats were randomly divided into normal group, CO poisoning group and NBP treatment group (n=20). Rats in CO poisoning group and NBP treatment group were induced acute CO poisoning in hyperbaric chamber and received hyperbaric oxygen therapy. Meanwhile, rats in the NBP treatment group were subjected to oral NBP 6 mg/100 g twice a day additionally. The expressions of Nogo, MAG and NgR1 were investigated in rat brain tissues by immunohistochemistry and double immunofluorescence staining 1 day, 3 days, 1 week and 4 weeks after CO exposure. Results With the prolongation of CO poisoning, the levels of Nogo, MAG and NgR1 in brain tissues of the CO poisoning group were gradually increased, and their expressions could still be detected at 4 weeks after CO poisoning. NBP treatment group had significantly reduced Nogo and NgR1 protein levels, and statistical differences were noted as compared with those in the CO poisoning group at each time point (P 0.05). Conclusions The levels of Nogo, MAG and NGR1 proteins may be associated with brain injury and demyelination induced by CO poisoning. NBP can downregulate the levels of Nogo and NgR1 proteins (but not MAG), and may play a neuro-protective role in brain damage after acute CO poisoning. Key words: Carbon monoxide poisoning; N-Butylphthalide; Neurite outgrowth inhibitor; Myelin-associated glycoprotein; Nogo receptor-1

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 call

Disclaimer: 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.