褪黑素对丙烯酰胺大鼠神经毒性拮抗作用

目的 探讨褪黑素(MT)同时干预对丙烯酰胺(ACR)神经毒性作用的影响。方法 40只SD雄性大鼠按体重随机分为4组,每组10只,分别为对照组、丙烯酰胺、褪黑素与褪黑素干预组,丙烯酰胺2.3 mmol/L溶液日常饮用;褪黑素腹腔注射2.5 mg/kg1,次/d,连续9周。每周进行步态评分,试验结束后取出大脑、小脑检测抗氧化指标。结果 与对照组比较,丙烯酰胺组与褪黑素干预组第3周开始步态分值明显升高,丙烯酰胺组大脑皮层SOD活性降低9.89%,小脑SOD活性、GSH含量分别降低7.49%1、2.31%,差异均有统计学意义(P<0.05);与丙烯酰胺组比较,褪黑素干预组第4、5周步态分值分别下降22.92%、15.85%,大脑皮层SOD活性升高14.96%,差异均有统计学意义(P<0.05)。结论 丙烯酰胺能导致大鼠步态改变,脑组织SOD活性及GSH含量降低。褪黑素对丙烯酰胺毒性早期有一定缓解作用,后期不明显。

Interference effect of melatonin on acrylamide-induced neurotoxicity in rats

Objective To explore the interference effect of melatonin on acrylamide-induced neurotoxicity in rats.Methods Forty adult male SD rats were randomly divided into control group,acrylamide group,melatonin group,and melatonin intervention group(10 in each group).Acrylamide group was treated with 2.3 mmol/L of acrylamide in daily drinking.Rats in melatonin group were administered 2.5 mg/kg of melatonin by intraperitoneal injection once a day.All the treatments continued 9 weeks.Gait scores were analyzed once a week.The histopathologial injuries of cerebrum and cerebellum were observsed by hematoxhlin-eosin(HE) stain.The contents of of malondialdehyde(MDA),glutathione(GSH),superoxide dismutase(SOD),and glutathione peroxidase(GSH-Px) in cerebral cortex and cerebellum tissue were determined.Results Compared with the control group,the gait scores rised markedly from the third week to the end of experiment(P<0.05) in acrylamide group and melatonin intervention group.In acrylamide group,the SOD activity in cerebral cortex decreased by 9.89%(P<0.05) and the SOD activity and GSH content in cerebellum decreased by 7.49% and 12.31%,respectively(P<0.05).Compared with acrylamide group,gait scores decreased at forth and fifth week by 22.92% and 15.85%,respectively(P<0.05),and the SOD activity in cerebral cortex increased by 14.96% in melatonin intervention group(P<0.01).Conclusion Acrylamide could induce gait abnormality,inhibit the activity of SOD and the content of GSH,while melatonin could alleviate the neurotoxicity induced by acrylamide at the early stage but have no protective effect later in rats.