肿瘤坏死因子会导致小鼠视神经中蛋白质的轴突运输增加以及脱髓鞘。
Tumour necrosis factor causes an increase in axonal transport of protein and demyelination in the mouse optic nerve.
作者信息
Jenkins H G, Ikeda H
机构信息
Vision Research Unit, Sherrington School (UMDS), Rayne Institute, St. Thomas' Hospital, London, U.K.
出版信息
J Neurol Sci. 1992 Mar;108(1):99-104. doi: 10.1016/0022-510x(92)90194-p.
Abstract
An increase in fast axonal transport of protein by the optic nerve was found in mice following a single combined injection of human recombinant tumour necrosis factor alpha (rTNF) and [3H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at least some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.
摘要
在向小鼠玻璃体内单次联合注射人重组肿瘤坏死因子α（rTNF）和[3H]脯氨酸后，发现小鼠视神经中蛋白质的快速轴突运输增加。在接受单次rTNF注射的小鼠眼睛发出的视神经纤维中观察到脱髓鞘现象。当热灭活的rTNF与标记物一起注射时，未检测到此类变化。玻璃体内注射rTNF对小鼠视神经病理生理学的影响与感染塞姆利基森林病毒（SFV，一种多发性硬化症动物模型）的小鼠中发现的影响相似。我们认为，TNF可能介导了在感染SFV的小鼠中发现的至少一些病理生理变化，并可能为多发性硬化症的疾病机制提供线索。
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