正己烷灌胃致周围神经病大鼠的神经行为和神经电生理异常变化

Abnormal changes of neurobehavioral and neurophysiological of peripheral neuropathy rats induced by n-Hexane

关键词:  正己烷  慢性暴露  神经行为  神经电生理  周围神经病

Key words:  n-Hexane  chronic exposure  neurobehavioral  neurophysiological  peripheral neuropathy

摘要:

目的　观察正己烷灌胃大鼠的神经行为和神经电生理异常变化，为复制正己烷诱导的周围神经病大鼠模型提供依据。 　方法　SD大鼠40只，随机分为4组，对照组，低剂量组，中剂量组和高剂量组每组10只。低剂量组，中剂量组和高剂量组以正己烷行灌胃，染毒剂量分别为132，527，2 109 mg/kg，对照组以生理盐水进行灌胃，1次/d，每周5 d，共染毒18周。在染毒过程中，观察大鼠的一般状态、体重和步态变化，并用肌电图与诱发电位仪检测各实验组大鼠尾神经AB两点间远端潜伏期DL（AB），AC两点间远端潜伏期DL（AC）和运动神经传导速度(MCV)。 　结果　与对照组相比，正己烷染毒大鼠的体重随染毒时间呈进行性下降。神经行为学观察结果显示，随染毒时间的延长，染毒大鼠出现周围神经病特有的异常步态，到染毒18周时各实验组大鼠异常步态加重，其神经行为评分值分别为2.00±0.00，2.60±0.52和2.90±0.32，明显高于对照组（P<0.01）。神经电生理指标显示，第12周染毒大鼠出现尾神经传导潜伏期 (DL)增加和MCV降低。到第18周，高剂量组大鼠尾神经远端潜伏期明显增加而传导速度明显减慢，与同时期对照组相比，DL（AB）和DL（AC）分别增加了65.39% (P<0.01)和79.90% (P<0.01)，而MCV则降低了39.50% (P<0.01)。　结论　通过消化道慢性暴露正己烷能导致大鼠的神经行为和神经电生理异常变化，正己烷灌胃可诱导大鼠周围神经病。

Abstract:

Objective　To observe the abnormal changes of neural behavioral and neurophysiological of rats treated by n-hexane in gavage (ig), to provide the evidence for the production of the peripheral neuropathy model in rats induced by n-hexane.　Methods　Forty SD rats were randomly divided into four groups evenly, and the rats were given 0、132、527、2109 mg/kg n-hexane for 18 weeks (5 d/w) ig. The general state, gait and weight changes of the rats were observed, alos distal latency（AB）, distal latency（AC）and motor nerve conduction velocity (MCV) of rats tail nerve was detected by the EMG-EP.　Results　Compared with the control, the weight of rats exposed to n-hexane decreased progressively with prolonged exposure. Neurobehavioral observations show that with the increase of exposure time, abnormal gait peculiar to peripheral neuropathy occurred in the each experimental rats. At 18 weeks, the gait scores of rats exposed to n-hexane were 2.00±0.00，2.60±0.52 and 2.90±0.32，which were significantly higher than the control group (P<0.01). At 18 weeks, the distal latency between point A and point B or C of rat tail nerve in high dose group increase significantly but MCV decrease significantly. Compared with concurrent control group, DL (AB) and DL (AC) were increased by 65.39% (P<0.01) and 79.90% (P<0.01), but MCV decreased by 39.50% (P<0.01). 　Conclusion　The rats chronic exposure to n-hexane can cause the abnormal changes of neurobehavioral and neurophysiological. The results suggest that peripheral neuropathy model could be successfully duplicated in the rats exposed to n-hexane.