Effect Of Edaravone Plus Hyperbaric Oxygen On Serum MDA Level, SOD Activity And Hippocampal CA1Area Neuron Apoptosis In Mice With Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

Patients may appear delayed encephalopathy after acute carbon monoxidepoisoning (DEACMP) with dementia, psychiatric symptoms, and extrapyramidalsymptoms as the main performance, which develops later following a symptom-free intervalof a few days or a few weeks. So far, there is no effective treatment. The clinical treatmentfor DEACMP includes utilizing of hyperbaric oxygen (HBO), reducing of cerebraledema, scavenging free radicals, improving cerebral perfusion and neuroprotection. Themechanism of DEACMP is still not entirely clear. Research primarily considered thatacute ischemia and hypoxia, cytotoxic injury, reperfusion injury and free radicals,excitatory amino acids and cell apoptosis, immune dysfunction and other relateddisorders of neurotransmitters might involved after carbon monoxide poisoning.HBO is the main method as clinical treatment of DEACMP. Edaravone has theneuro-protective function as a potent scavenger of free radicals and antioxidants. Theexperimental study related to the treatment of edaravone plus hyperbaric oxygen onDEACMP has not been reported.Objective:To investigate the effect of edaravone plus hyperbaric oxygen(HBO) on MDAlevel, SOD activity in serum and the apoptosis of hippocampal CA1area in mice withdelayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods:72Kunming mice were randomly divided into6groups with12rats each group:control group, DEACMP group, saline group, HBO group, edaravone group andedaravone plus HBO group(EPH). The animal model of DEACMP were established byinjection of high-dose CO intraperitoneally in mice. The saline group were injected withnormal saline through intraperitoneal. Hyperbaric oxygen group were treated with HBO.Edaravone group were treated with intraperitoneal injection of edaravone. Besidesreceiving same HBO treatement as the HBO group, EPH group were also treated withintraperitoneal injection of edaravone. After treatment, serum MDA levels, SODactivity and hippocampal neuron apoptosis of CA1area were measured in each group.Results:1)Serum MDA levels were higher and SOD activity in DEACMP group wassignificantly lower than that in the control group (P﹤0.05). Except the saline group,Serum MDA levels in other treatment groups were lower and SOD activity in othertreatment groups were higher than that in DEACMP group (P﹤0.05). Serum MDAlevels were lower and SOD activity in EPH group was higher than that in HBO groupand edaravone group(P﹤0.05);2)There were several apoptotic cells occasionally inhippocampal CA1area in control group.Except saline group, the apoptotic index inother treatment groups were lower than that in DEACMP group (P﹤0.05); theapoptotic index of HBO group and edaravone group were higher than that in EPH group(P﹤0.05).Conclusion:Edaravone plus HBO can reduce MDA levels and increase SOD activity, and alsosignificantly inhibit the neuronal apoptosis in hippocampal CA1area.The effect of edaravone plus HBO is better than that of HBO treatment and edaravone group.