Change in neurite outgrowth inhibitor-A and injury of corpus callosum of rats with delayed neuropsychologic sequelae after acute carbon monoxide poisoning

doi:10.3969/j.issn.1002-1949.2014.08.22

Abstract：Objective To investigate the change in neurite outgrowth inhibitor -A ( Nogo-A) and injury of the corpus callosum of rats with delayed neuropsychologic sequelae ( DNS ) after acute carbon monoxide (CO) poisoning.Methods Healthy Male SD rats were divided into control group and poisonous group randomly .Poisonous group was given intraperitoneal injections of CO to make models of DNS.Corpus callosum was taken from the poisonous rats at 0 h, 12 h, 24 h, 3 d and 7 d after successful modeling , and the sample for control group was paralleled taken at the same time points .HE staining was performed to observe the changes of cellular morphology .Chromotropic acid staining was used to observe myelin changes .Immunohistochemical method was used to observe the expression of Nogo-A.The mRNA levels of Nogo-A at 0 h, 12 h, 24 h, 3 d and 7 d of poisonous group and control group were detected by real -time quantitative polymerase chain reaction ( RT -PCR ) . The ultrastructure was observe under the electron microscope .Data was analyzed with SPSS17.0.Results The rats in poisonous group appeared leukoaraiosis and neuron pyknosis by HE staining , and white matter demyelination by chromotropic acid staining .The most significant damage was shown in 0 h group of successful modeling and over time we found a mitigation of the injury by two staining methods . Immunohistochemical results showed that Nogo -A expressed all the time in poisonous group while its expression on day 3 began to decline .RT -PCR results showed that Nogo -A mRNA expressed in normal corpus callosum .The mRNA level of Nogo -A increased at the 0 h and lasted to 24 h.Its expression reached a peak at 0 h.The expression of Nogo -A mRNA began to decrease on day 3, which declined near the control group .On day 7, the level of Nogo -A mRNA rose again.Myelin shelf structure loose solution , fusion and fracture were observed in the corpus callosum while the density of axone was thin of poisonous group under the electron microscope .Conclusion Demyelination injury characterized by corpus callosum appears immediately after acute CO poisoning .The degrees of injury changes over time .Nogo-A mRNA expresses in normal corpus callosum , and it is up-regulated at 0 h and rose again on day 7 of CO poisoning .Our findings demonstrated that Nogo -A might be involved in demyelination injury after acute CO poisoning .