Delayed encephalopathy of acute carbon monoxide intoxication in rats: potential mechanism and intervention of dexamethasone.

We aimed to investigate the potential mechanism (s) of delayed encephalopathy after acute carbon monoxide (CO) poisoning in rats, and the effect of dexamethasone on this process. A delayed encephalopathy animal model was generated by intraperitoneal injection of CO into Wistar rats. Normal rats were sent as a control group, and poisoning rats were randomly separated into two groups treated with vehicle and dexamethasone respectively. The rat behavior was evaluated by Morris water maze. The level of myelin basic protein (MBP), myeloperoxidase (MPO) expression in the serum and hippocampus of experimental rats was measured using enzyme-linked immunosorbent assay (ELISA) and immunohisto chemistry. The latency to find the platform was significantly increased by dexamethasone treatment for rats after poisoning at day 7 and 14. MBP serum concentration in the vehicle treatment group was significantly higher than that in rats injected with dexamethasone following poisoning at 90 min, 7d, 14d, 21d. Moreover, MPO concentration was higher at day 14 after poisoning as well. In addition, MBP expression was down regulated in the poisoning group, which was nearly reversed at control level in the dexamethasone group. Inflammation plays a key role in delayed encephalopathy of rats induced by acute CO intoxication, which could be attenuated by dexamethasone via protecting myelin from damage of inflammation response.