Abstract

Objective To investigate the effect of hyperbaric oxygen (HBO) therapy on the expression of nitric oxide synthase (NOS) mRNA in hippocampus following acute traumatic cerebral injury, and also to study the mechanism of HBO on brain injury.Methods Acute traumatic cerebral injury model was established with restricted free fall injury method in Sprague-Dawley rats. HBO therapy at a pressure of 0.25 MPa was administered 1 h or 12 h after brain injury and samples were taken from hippocampus CA1 areas 6 h and 24 h after brain injury respectively. Changes in the expression of mRNA coding for iNOS or nNOS were monitored by using half-quantitative reverse transcription polymerase chain reaction (RT-PCR).Results The expression of iNOS mRNA and nNOS mRNA decreased significantly in the 0.25 MPa HBO therapy group than that of the acute cerebral injury groups (P 0.05).Conclusions Changes in the expression of nNOS at the initial stage of acute traumatic cerebral injury might induce toxication, while the expression of iNOS at the later stage of acute traumatic cerebral injury might induce toxication. HBO therapy seemed to reduce the production of NO and hippocampus neurons might thus be protected, following acute traumatic cerebral injury. Key words: Hyperbaric oxygen; Acute traumatic cerebral injury; Hippocampus; Nitric oxide synthase; Gene expression

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