RESUMO
Objective:Preliminary study on rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) model intervention agent tBHQ before and after the nuclear factor E2-related factor 2(Nrf2) and its downstream target genes of heme oxygenase 1(HO-1) change in hippocampus associated,in order to further study the pathogenesis of DEACMP,at the same time for the targeted therapy of provide a certain experimental basis.Methods: One hundred and twenty rats were randomly divided into carbon monoxide poisoning group(CO group),air control group(AC group),carbon monoxide+3% ethanol group(EC group),carbon monoxide+tBHQ group(group TC),then the rats in exposure after 1 d,3 d,7 d,14 d,21 d,28 d,with the machine was divided into 6 sub groups,followed by the Morris water maze test to observe the behavior of rats,immunohistochemistry and protein Western blot method of chemical(Western blot) detecting expression of Nrf2 and HO-1 mploying intervention agent tBHQ before and after,and then TUNEL staining was detected cell apoptosis.Results: CO group,EC group,TC group Nrf2 in hippocampus of rats and the expression of HO-1 were increased in the first day and reach a peak at the third day,then gradually decreased,and at each time point in AC group were statistically significant,TC group and CO group Nrf2 and HO-1 were increased in each sub group and the deffirences were statistically meaning.Comparison apoptotic cells in CO group,EC group,TC group with AC group rats increased significantly over time,and showed higher peak(7-14 d)-decreased.TC group compared with CO group,the apoptotic cells(7-14 d) decreased,the difference was statistically significant.Conclusion: The Nrf2/ARE/HO-1 pathway plays an important role in the development of DEACMP,and the tBHQ specific activation of the Nrf2 pathway achieves early protection and is expected to reduce or mitigate DEACMP.