RESUMEN
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 90min, 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
RESUMEN
OBJECTIVE: To observe the mouse nerve growth factor on early intervention in rats with acute carbon monoxide intoxication delayed encephalopathy control effects, and preliminarily discuss the pathogenesis of delayed encephalopathy. METHODS: Ninety-two weight only 180-230 g, male Wistar rats were randomly divided into two experimental groups (n=40), and a healthy control group (n=12), namely the CO poisoning group (COP) of the group; mouse nerve growth factor (NGF plays group); healthy controls (NC group). Experimental group was according to 150 mL·kg-1 intraperitoneal injections of CO in the preparation of animal model of acute carbon monoxide poisoning, in the control group rats were injected with equal volume of air. NGF group rats were injected within 30 min after poisoning muscle injection of mouse nerve growth factor, once a day, every time 18 μg·kg-1, total 7 days; Control group and the COP were given intramuscular isodose physiological saline. NGF group rats were treated with 18 μg·kg-1·d-1 NGF (total 7 times); NC group and COP group treated with the same dose saline. 90 min, 7 day, 14 day and 21 day groups of rats serum myelin basic protein (MBP) levels were monitored. The routine preparation of brain tissue frozen pathology slice, line HE and MBP immunohistochemical staining. Animal intelligence is assessed by Morris water maze experiment, in the 120 s in rats to determine correctly through the platform number less than 3 times DEACMP. RESULTS: All rats showed typical toxic after CO poisoning. Experimental group rats died 29, including COP death cases in the group, the model NGF group of 15, 14, mortality rates were 37.50%, 35.00% respectively. Morris water maze experiment results showed that the COP in the group 8 rats were judged to be delayed encephalopathy; model NGF group has 5 only be judged to be delayed encephalopathy; COP group rats serum MBP content increased significantly, model NGF group close to normal.Differences were obvious in poisoning after 7 days, 14 days.Pathological examination showed the COP group delayed encephalopathy rats in poisoning 90 min-21 d in hippocampus, subcortical neurons damage, such as myelin basic protein depigmentation pathological changes.The above pathological changes can be observed in each group, the COP group rats lesion severity is heavy, model NGF group was lighter. CONCLUSION: Mouse nerve growth factor can significantly reduce the incidence of delayed encephalopathy in rats, but can't reduce the mortality. Myelin basic protein (MBP) in the pathogenesis of delayed encephalopathy may play an important role.