Saita K, Ohi T, Hanaoka Y, Furukawa S, Furukawa Y, Hayashi K, Matsukura S
Department of Internal Medicine, Miyazaki Medical College, Japan.
J Pharmacol Exp Ther. 1996 Jan;276(1):231-7.
Acrylamide (ACR) monomer produces neuropathy of the dying-back type and 4-methylcatechol (4-MC) is a potent stimulator of endogenous nerve growth factor synthesis. In the present study, we investigated the efficacy of 4-MC in promoting recovery from experimental ACR neuropathy in rats. Twenty-two Sprague-Dawley rats were made neuropathic by ACR injections. They showed hindlimb paralysis, increment of landing foot spread distance and a statistically significant reduction in motor nerve conduction velocity. After the ACR neuropathy had been established, 12 of the rats were administered 4-MC for 2 weeks, and the other 10 were injected with phosphate-buffered saline alone. 4-MC-administered ACR neuropathy rats showed improvement, i.e., a decrease in landing foot spread distance, increase in motor nerve conduction velocity and increase in nerve growth factor content in the sciatic nerves in comparison with the corresponding values for ACR neuropathy rats given phosphate-buffered saline alone. A decreased number of large myelinated fiber with a reciprocal increase in small myelinated fiber number also was seen in the ACR neuropathy rats; however, this change was ameliorated in part by the administration of 4-MC. Therefore, these findings suggest that 4-MC can accelerate the recovery process clinically, electrophysiologically, biochemically and neuropathologically.
丙烯酰胺(ACR)单体可引发轴突逆行性变性的神经病变,而4-甲基邻苯二酚(4-MC)是内源性神经生长因子合成的强效刺激剂。在本研究中,我们探究了4-MC对促进大鼠实验性ACR神经病变恢复的效果。通过注射ACR使22只Sprague-Dawley大鼠发生神经病变。它们出现后肢麻痹、着地脚间距增加,且运动神经传导速度有统计学意义的降低。在ACR神经病变形成后,给12只大鼠给予4-MC,持续2周,另外10只仅注射磷酸盐缓冲盐水。与仅给予磷酸盐缓冲盐水的ACR神经病变大鼠的相应值相比,给予4-MC的ACR神经病变大鼠表现出改善,即着地脚间距减小、运动神经传导速度增加以及坐骨神经中神经生长因子含量增加。在ACR神经病变大鼠中还可见大髓鞘纤维数量减少,小髓鞘纤维数量相应增加;然而,给予4-MC可部分改善这种变化。因此,这些发现表明4-MC可在临床、电生理、生化和神经病理学方面加速恢复过程。