摘要
目的:研究不同发病时期实验性变态反应性脑脊髓炎(EAE)大鼠轴索损伤的动态变化及意义。方法:对不同发病时期EAE大鼠进行HE染色判断炎症损害,以免疫组化方法标记β-淀粉样前体蛋白(β-APP)和磷酸化tau蛋白,了解轴索急性损伤及反复发病后的神经变性情况。结果:急性组大鼠脊髓组织内可见大量炎症细胞弥散分布,在炎症细胞区内有大量β-APP阳性表达,神经纤维变性标志物tau蛋白只有少量沉积;瘫痪组大鼠血管周围有淋巴细胞浸润,呈袖套样分布,β-APP在无炎症的区域也有部分表达,并有tau蛋白大量沉积,提示反复发病的瘫痪大鼠存在持续的轴索损伤,并发生明显的轴索变性。急性组、瘫痪组轴索中β-APP和tau蛋白阳性数均多于正常组,差异显著,急性组和瘫痪组比较,轴索中β-APP和tau蛋白阳性表达数亦有显著差异。结论:(1)发病早期轴索损伤与炎症破坏有关,并呈可逆性。(2)神经变性主要存在于EAE的慢性病程中。(3)在EAE发病过程中轴索损伤呈动态变化,疾病后期轴索发生神经变性并导致神经功能不可逆损伤,在EAE研究中有重要意义。
AIM： To study the dynamic changes and significance of axon damages in different stages of experimental allergic encephalomyelitis（EAE）.METHODS： Tissue sections were processed with HE staining to observe inflammatory damages.The expression and distribution of β-amyloid precursor protein（β-APP） and tau protein were detected by the method of immunohistochemistry in acute and relapsing-remitting stages of EAE.RESULTS： Many inflammatory cells were infiltrated in the tissues of spinal cord and strong β-APP expression was observed in the area full of inflammatory cells in acute EAE rats.Meanwhile,a small amount of tau protein,the marker of neurodegeneration,was found.There were many perivascular cuffings in the tissues enclosed by the inflammatory cells,and there was also strong β-APP expression in the tissues where there was no inflammatory cell infiltration in paralyzed rats.Tau protein also largely precipitated in the spinal tissues of paralyzed rats with the repeated episodes,indicating that persistence of axon damages and evident axon degeneration existed.Positive cells of β-APP and tau protein in acute group and relapsing-remitting group were larger than those in normal group with statistical differences.A statistical difference between acute group and relapsing-remitting group was also observed.CONCLUSION： Axon damages are concerned with inflammation in the spinal cord.Axon damages accompany with neural degeneration during the process of chronic EAE.The permanent damages of axon are in the course of EAE.The degeneration of axon happens in the late time of relapsing-remitting EAE and results in irreversible neurological deficits.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2011年第12期2407-2410,2428,共5页
Chinese Journal of Pathophysiology
基金
河北省卫生厅科技攻关项目(No.08107)
