突触素I在丙烯酰胺大鼠亚急性神经损伤中的变化

Study on changes of synapsin I in acrylamide-induced subacute neurotoxicity in rats

目的探讨突触素I(synapsin I)在丙烯酰胺(acrylamide,ACR)大鼠亚急性神经损伤中的变化。方法 48只Wistar大鼠,雄雌各半,腹腔注射ACR染毒(7.5、15和30 mg/kg ACR),生理盐水(normal saline,NS)对照;步态评分评价神经行为改变;电子显微镜检测脊髓神经突触的改变;免疫组化法检测synapsin I的定性、定位改变,Western-blot检测synapsin I的定量变化。结果染毒结束时,30 mg/kg ACR染毒组大鼠体重较对照显著减轻,突触数量较对照显著减少,步态评分较对照显著增加(P<0.05);对照组和ACR各剂量染毒组synapsin I的定位一致,均位于脊髓背角灰质;对照组脊髓背角灰质神经纤维末梢synapsin I呈强阳性反应,随染毒剂量增加该阳性信号减弱;30 mg/kg ACR组synapsin I蛋白表达显著降低(P<0.05)。结论 synapsin I在ACR亚急性神经损伤中的变化显著,与神经行为及神经病理学变化相符,可能是ACR神经突触损伤的作用靶点之一。

Objective This study was aimed to explore the changes of synapsin I in acrylamide-induced subacute neurotoxicity in rats. Methods Forty-eight Wistar rats were divided into control and test groups randomly. The ratio of male and female in each group was 1：1. Different concentrations of ACR （7.5, 15 and 30 mg/kg） were administered to Wistar rats by intraperitoneal injection in treatment groups and normal saline was given to rats in the control group. Changes of weight and behavior were observed. Gait scores were noted. Synapses were examined by electron microscopy. As an important target of synapse, changes of synapsin I were measured by immunohistochemical and western-blot. Results Weight of rats treated with 30 mg/kg ACR was decreased compared with the control group at the end of the test （ P 〈 0.05 ）. Neurobehavioral changes were significant at the third week of the treatment. Gait score of rats in 30 mg/kg ACR treatment group was higher than that of the control group, numbers of synapse of 30 mg/kg ACR treatment group was lower than that of the control group （ P 〈 0.05 ）. The location of synapsin I in control group and ACR treated group was both in gray matter of the spinal dorsal horn. Compared with the control group, the level of synapsin I was decreased significantly in 30 mg/kg ACR treatment group （P 〈 0.05 ）. Conclusion Changes of synapsin I was sensitive in ACR-induced subacute neurotoxicity and was consistent with the changes of behavior and pathology. Synapsin I might be one of the targets of ACR-induced subacute neurotoxicity.