Carbon monoxide (CO) intoxication is one of the most common types of
poisoning worldwide, and may result in neuropathologic sequelae, yet its pathogenesis is not clear and there is no optimal management strategy for patients with CO
poisoning. In this study, the rat model of CO
poisoning was established in a hyperbaric chamber by CO exposure. Rats were administered orally
N-Butylphthalide (NBP) at a dose of 1 ml/100g. Neuronal apoptosis was assessed by TUNEL
stain and flow cytometry. The expressions of neurite outgrowth inhibitor (Nogo),
myelin-associated glycoprotein (MAG) and Nogo receptor-1 (NgR1) were observed in rat brain tissue by immunohistochemistry and double immunofluorescence staining. As we expected, CO
poisoning could start the mechanism of apoptosis. The number of apoptotic cells and the early neuronal apoptosis percentage (EAR) were significantly increased at 1 day, 3 day after CO exposure. NBP treatment obviously reduce neuronal apoptosis and the EAR (P<0.05). CO
poisoning could induce Nogo, MAG and NgR1 expressions. The increased Nogo, MAG and NgR1
proteins were still observed at 4 week after CO
poisoning. NBP could significantly reduce the levels of Nogo and NgR1
proteins. Then we suspected that the expressions of Nogo, MAG and NGR1
proteins might be associated with
brain injury and
demyelination induced by CO
poisoning. NBP might inhibit neuronal apoptosis and the EAR, down-regulate the expressions of Nogo and NgR1
proteins (but not MAG), and play a neuro-protective role in brain damage after acute CO
poisoning.