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Effect of rhTNF-alpha injection into rat sciatic nerve.

机译:rhTNF-α注射到大鼠坐骨神经中的作用。

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摘要

To assess whether TNF-alpha causes inflammatory demyelination or axonal degeneration, we injected into rat sciatic nerve saline, 100 U and 1000 U of rhTNF-alpha and studied the electrophysiological and pathological effects. At day 1 electrophysiology showed a slight reduction of proximal compound muscle action potential amplitude and pathology showed edema, inflammatory infiltration of vessel walls and endoneurium only in nerves injected with 1000 U of rhTNF-alpha. At day 5, there was no demyelination and a percentage of degenerated fibers similar in the three groups. To study the blood-nerve barrier, fluorescein isothiocyanate-labelled albumin was given intravenously after intraneural injection. The nerves injected with 1000 U rhTNF-alpha showed a leakage of the tracer in the endoneurium. TNF-alpha does not appear, at the doses used, to have myelinotoxic or axonopathic properties. The electrophysiological effect at day 1 may be due to mechanical compression of nerve fibers as a result of the blood-nerve barrier damage with consequent endoneurial edema.
机译:为了评估TNF-α是否引起炎症性脱髓鞘或轴突变性,我们向大鼠坐骨神经生理盐水,100 U和1000 UrhTNF-α注射,并研究了其电生理和病理学作用。在第1天,电生理学显示,仅在注射1000 UrhTNF-α的神经中,近端复合肌动作电位幅度略有降低,病理学显示浮肿,血管壁和神经内膜的炎性浸润。在第5天,三组中没有脱髓鞘,并且百分数的变性纤维相似。为了研究血液神经屏障,在神经内注射后静脉内注射荧光素异硫氰酸酯标记的白蛋白。注射1000 UrhTNF-α的神经在示踪神经内膜中示踪剂泄漏。在所使用的剂量下,TNF-α似乎没有髓系毒性或轴索变性。第1天的电生理效应可能是由于神经纤维受到机械性压迫所致,其原因是血液神经屏障受损并伴有神经内膜水肿。

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