慢性实验性变应性脑脊髓炎猴脊髓非病灶部位轴突损伤的机制

【目的】探讨多发性硬化非病灶部位轴突损伤及其机制。【方法】以8只慢性实验性变应性脑脊髓炎猴为研究对象,先对其进行磁共振扫描,然后对颈髓3-4节段进行苏木素-伊红染色观察炎症细胞浸润、银染色及神经丝免疫组化染色观察轴突损伤、双重染色标记凋亡的少突胶质细胞,同时观察轴突密度以及少突胶质细胞的凋亡情况。【结果】在颈髓3-4节段未发现有实验性变应性脑脊髓炎病灶、炎症细胞浸润及髓鞘脱失,但是存在轴突损伤以及少突胶质细胞的凋亡,轴突密度波动于1900～3232/单位面积,高倍视野下平均凋亡少突胶质细胞数为1.5～5.167。【结论】造成多发性硬化或实验性变应性脑脊髓炎非病灶部位轴突损伤的机制,可能与少突胶质细胞凋亡有关,而炎症细胞可能不参与非病灶部位的轴突损伤,髓鞘脱失并不是轴突损伤的必要条件。

Mechanism of Axonal Injury in Nonlesion Areas of Spinal Cord of Monkey with Chronic Experimental Allergic Encephalomyelitis

Objective To investigate axonal injury and its mechanism in the nonlesion areas of multiple scler-osis(MS).Methods Firstly,magnetic resonance imaging was performed on 8 monkeys with chronic experimental allergic encephalomyelitis(EAE).Secondly,all of them were killed and slices from their No.3-4 cervical segment were stained with haematoxylin-eosin(HE)for inflammatory cells,modified Bielschowsky sliver impregnation and neurofilament immunohistochemical staining for axons,double staining for the apoptotic oligodendrocytes.Mean-while,axonal density and apoptotic oligodendrocytes were detected.Results Lesions,inflammatory cells and the loss of myelin sheath were not detected in the No.3-4 cervical segment,but there existed the axonal injury and apoptotic oligodendrocytes.The mean axonal density ranged from 1900 to 3232 per unit area,and mean apoptotic oligodendrocytes from 1.5 to 5.167 per one high power field.Conclusion The mechanisms contributing to the axonal injury in the nonlesion areas of EAE and MS maybe include the apoptosis of oligodendrocytes,but not the inflammatory cells.The loss of myelin sheath is not the prerequisite of axonal injury.