| Objective:The Experimental Allergic Encephalom- yelitis(EAE) is the most suitable animal model for investigation of the pathogenesis and the treatment of EAE.Multiple clinical processes on experimental allergic encephalomyelitis model was the research foundation of the study and detected the expressions and distributions of Nestin which was the marker of neural stem cells and BrdU which was the marker of caryocinesia.Furthermore the study inspected reaction of neural stem cells to injury and detect the purpose and significance of the neural stem cells in the repairation of the injuried brain.Methods:The animal model was established in Wistar rat by immunizalion with complete Freund adjuvant and GPSCH.The pathological changes of EAE studied with the aid of light microscopy by HE staining and Nerve myelin special staining,observered the expressions and distributions of Nestin and BrdU by Immunohistochemistry and Results:EAE model showed typical clinical situation pathological change and ultrastructure of EAE. Results:We can divide the EAE into five types by pathological changes and clinical manifestation:acute EAE, relapsing-remitting EAE,persistent progress EAE,benigh form EAE and delitescence EAE.And two compare groups:normal group and Phase disease. Histological changes:HE staining:â‘ The total cells of SVZ in relapsing-remitting EAE ,benigh form EAE and delitescence EAE and morbility EAE were statistically significant higher than acute EAE and control group(P<0.05) ,but acute EAE and persistent progress EAE had no statistical differences with control group (P>0.05).â‘¡Every type mainly congestion and inflammatory cuff of small blood vessels,disintegration and disappear of myelin sheath and degeneration of neurons.â‘¢District lesions strictly distributed in the area surrounded by lateral ventricle,corpus callosum,and optic chiasma.Immunohistochemistry(IH) staining,â‘ nestin:Nestin was mainly expressed in SVZ,district lesions(anterior commissure,corpus callosum,and optic chiasma) and (OVLT,SFO,ME)The nestin positiveness cells had different morphous,which were round ,ellipse,or triangle and had big nucelus , little endochylema cladodromous,which were cladodromous, had different sizes and processes, the processes were closely linked with vascular wall.There was single processe in OVLT and ME. With the pathogenetic condition improved,the nestin positiveness cells were decreased ,even disappeared.There were no nestin positiveness cells founded in dentate gyrus of the hippocampus There were no statistical differences between acute EAE and control group in SVZ.(P>0.05) .Morbility EAE were statistically significant higher than acute EAE and control group(P<0.05).The average of nestin positiveness cells had the relations:persistent progress EAE>Morbility EAE >relapsing-remitting EAE>control group there were statistically significant differences (P<0.05);Control group had no statistical differences with benigh form EAE and delitescence EAE (P>0.05).â‘¡BrdU:There was only a expression of SVZ ,a weak expression of dentate gyrus of the hippocampus in control group.In the EAE modle,the expression of BrdU was increased ,the average of BrdU positiveness cells had the relations:Morbility EAE >acute EAE >persistent progress EAE>control group there were statistically significant differences (P<0.05);another groups had no statistical differences with control group(P>0.05)Conclusions:â‘ Muihple clinical processes on EAE model of Wistar rat were established as an ideal animal model in studying MS.â‘¡The total cells of SVZ in the progress of EAE remained high level and had proliferation and differentiation which was beneficial for the prog of EAE.â‘¢Neural stem cells of SVZ were not directly migrated to the district injury.â‘£The nestin positiveness cells had different morphous in subventricular zoon ,circumv- entricular organs and district lesions,only the nestin positiveness cells of SVZ had association with cells generation .This study suggested the nestin positiveness cells were not neural stem cells completely.
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