摘要
目的:建立一成功率高,感觉症状确实的感觉性神经元神经病的动物模型。并同时观察不同剂量维生素 B6对于大鼠感觉性神经系统的作用。方法:50只雌性Wistar大鼠分别给予600mg／kg(1周或2周),400mg／kg(4周), 200mg／kg(4周或8周)与100mg／kg(4周或8周)维生素B6,腹腔注射,每天一次。取其后根神经节(DRG),周围神经及脊髓作光镜与电镜分析。染色方法有HE,Luxol Fast Blue,Masson三色与银浸染色。半薄切片用甲苯胺兰染色,超薄切片用醋酸双氧铀与枸橼酸铅染色。结果:腰段DRG受累最重,其次为颈段、胸段。大剂量组导致感觉性神经元神经病,动物步态不稳,甚至瘫痪。DRG细胞体体积减少或坏死,伴以轴突萎缩与崩解,并可见吞噬细胞吞噬现象。小剂量组动物无异常临床表现,DRG神经元病变轻微,但存在轴突萎缩与变性。电镜下发现近端突与胞体均有细胞骨架异常。脊髓后束中薄束比楔束病变重。结论:多种因素包括用药时间、用药剂量及不同亚群神经元的药物敏感性不同,均可影响维生素B6神经毒性的最终表现。
Objective： Our purpose was to get a animal model of sensory neuronopathy and to examine the abnormalities of the nervous system that resulted when rats were given various amounts ofvitB6. Methods： Fifty female wistar rats were treated with 600mg/kg, 400mg/kg, 200mg/kg, 100mg/kg of pyridoxine respectively by intraperitoneal iniection once daily, and were killed at various time. Dorsal root ganglia（DRG）and their processes were processed for electron microscopy and light microscopy. Results： High doses of pyridoxine caused a neuronopathy with necrosis of DRG sensory neurons and formation of Nageotte nodules, accompanied by centrifugal axonal atrophy and breakdown of peripheral and central sensory axons . The lumbar DRG were preferentially affected. Smaller dose had miner effects on DRG neurons, but produced a neuropathy with axonal atrophy and degeneration. In the dorsal spinal columns, the gracile tract changed most. secondly, the cuneate tracts. By electron microscopy we found domains of altered cytoskeleton consisting of aggregates of N F or microtubules. Conclusion： From adbove we conclude that multiple tactors including doses and time of pyridoxine, differential neuronal vulnerability have bearing in the final expression of pyridoxine neurotoxicity. These findings established a simple and definite animal model for sensory neuronopathy.
出处
《脑与神经疾病杂志》
2006年第3期168-171,189,共5页
Journal of Brain and Nervous Diseases
