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目的研究恢复期不同预后缓解-复发型EAE大鼠轴索损伤与神经功能障碍之间的关系。方法按照发病情况把缓解-复发型EAE大鼠分为缓解组和瘫痪组,分别进行HE染色和改良的Bielschowsky轴索染色,以免疫组化方法标记脊髓白质轴索中Tau蛋白的表达。结果缓解组和瘫痪组大鼠脊髓组织内均可见多个血管周围炎性细胞浸润呈袖套样分布,改良的Bielschowsky银染色轴索成空泡样缺失。神经纤维变性标志物Tau蛋白在变性的轴索内沉积,呈阳性表达的轴索数在缓解组和瘫痪组均高于正常组,差异显著(P<0.01),瘫痪组轴索内Tau蛋白呈阳性表达的数量高于恢复组,差异显著(P<0.01),具有统计学意义。结论缓解-复发型EAE大鼠的组织病理学改变为炎性细胞浸润和轴索损伤;恢复期大鼠缓解组与瘫痪组均发生轴索变性,当损伤达到一定程度会发生临床不可逆性神经功能障碍,导致肢体瘫痪。
Objective To study the relationship between axonal injury and neurological dysfunction in different prognosis recuperation-relapsing EAE rats. Methods According to the incidence of remission, EAE rats were divided into remission group and paralysis group. HE staining and modified Bielschowsky axon staining were performed respectively. The expression of Tau protein was detected by immunohistochemistry in white matter axon. Results There were multiple perivascular infiltration of inflammatory cells in cuff-like distribution in the spinal cord of the remission group and the paralyzed group. The modified Bielschowsky silver-stained axon was vacuolar-like. Tau protein, a marker of neurofibrosis, was significantly higher in the remission group and the paralyzed group than in the normal group (P <0.01). The expression of Tau protein in the paralyzed group The number of positive expression was higher than that of recovery group, with significant difference (P <0.01), with statistical significance. Conclusions The histopathological changes of remitting EAE rats are inflammatory cell infiltration and axonal injury. Axonal degeneration is observed in the remission rats and paralyzed rats. When the injury reaches a certain level, clinical irreversible neurological function Obstacles, leading to paralysis of limbs.