中文摘要：

目的探讨钙蛋白酶抑制剂（calpeptin,CP）对丙烯酰胺（acrylamide,ACR）中毒大鼠神经毒性的拮抗作用。方法将30只健康成年雌性Wistar大鼠随机分为对照组、ACR中毒组、CP干预组3组,每组10只。ACR中毒组腹腔注射ACR30 mg/kg,3次/周,共4周;对照组腹腔注射等体积生理盐水;CP干预组腹腔注射ACR后1 h再腹腔注射CP 200μg/kg,3次/周,共4周。测定体重、步态评分、后肢撑力和神经组织细胞内钙蛋白酶（calpain）活力。结果与对照组相比,ACR中毒组大鼠体重增加缓慢（P〈0.05）;与ACR中毒组相比,CP干预组大鼠体重在第2周显著升高（P〈0.05）。ACR中毒组和CP干预组步态评分和后肢撑力明显高于对照组（P〈0.01）,CP干预组明显高于ACR组（P〈0.05）。ACR中毒组和CP干预组脊髓、坐骨神经细胞中calpain活力均明显高于对照组（CP干预组坐骨神经除外）;CP干预组脊髓、坐骨神经细胞中calpain活力明显低于ACR组（P〈0.05）。结论 CP可通过抑制钙蛋白酶的活力拮抗ACR诱导的神经毒作用。

英文摘要：

Objective To research the neuroprotective effect of calpeptin（CP） and to investigate the mechanism of neuropathy induced by acrylamide（ACR） by means of observing ACR poisoning symptoms remissions after the intervention therapy of CP.Methods Female adult Wistar rats were randomly divided into three groups（control group,ACR group and CP group,10 in each group）. Control group received 0.9% saline,and the other two groups received 30 mg/kg ACR by intraperitoneal（i.p.） injection.In addition,CP group also received 200 μg/kg CP. The general situation, gait analysis and hind limb splay were examined weekly to analyze the neurobehavioral changes. The activity of calpain of spinal cord and sciatic nerve were determined by using calpain substrate Ⅱ with fluorescence spectrophotometer. Results The gait score and the distances from the center of the right and left heels of rats in ACR group were increased compared with control group,while they were decreased（P〈0.05） in ACR ＋CP group compared with ACR group. Spinal cord and sciatic nerve calpain activity at ACR group was increased compared with control group,and was decreased（P〈0.05） in ACR＋CP group compared with ACR group. Conclusion CP can relieve neurotoxicity induced by ACR in rats. The mechanism may be connected with the inhibition of calpain.