摘要
目的观察PEP-1-铜、锌超氧化物歧化酶(PEP-1-SOD1)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)所致帕金森病小鼠行为学和氧化应激损伤的影响,探讨其可能的神经保护机制。方法 36只C57/BL小鼠随机分为正常组、模型组和PEP-1-SOD1组。模型组给MPTP腹腔注射,连续5 d;PEP-1-SOD1组连续腹腔注射MPTP5 d前给予PEP-1-SOD1腹腔注射3 d。通过爬杆实验观察小鼠行为学变化。取小鼠纹状体通过黄嘌呤氧化酶法检测铜/锌超氧化物歧化酶(SOD1)和谷胱甘肽过氧化物酶(GSH-Px)活性,通过TBA法检测MDA含量。结果模型组小鼠爬杆能力明显下降,PEP-1-SOD1组处理的小鼠行为学异常明显改善(P<0.01)。模型组小鼠纹状体SOD1和GSH-Px活性明显降低,MDA含量显著升高(P<0.01)。同模型组比较,PEP-1-SOD1组小鼠纹状体SOD1和GSH-Px活性显著增高,MDA含量明显减少(P<0.01)。结论 PEP-1-SOD1具有神经保护作用,其机制可能与减轻氧化应激损伤、增强抗自由基损伤能力有关。
Objective To investigate the effects of PEP-I-SOD1 on oxidative stress injury in mice with Parkinson＇s Disease induced by MPTP. Methods 36 C57/BL mice were randomly divided into normal group, model group and PEP-1-SOD1 group. The model group was established by intraperitoneal injection with MPTP daily for 5 days;while for the PEP-I-SOD1 group, the intraperitoneal injection of MPTP started after 3 days injection of PEP-I-SOD1. The behaviors of mice were tested through pole tests; the striatum were dis- sected for SOD1 and GSH-Px activity and MDA amount by spectrophotometer methods. Results Compared with normal group, the model group were more behavior disability, and the activity of SOD1 and GSH-Px in the model group were significantly lower, while the content of MDA were significantly higher（P〈0. 01 ）. The PEP-1-SOD1 group had significantly improved in the different indexes（P〈0. 01）. Conclusions PEP-1-SOD1 shows neuroproteetion in mice with Parkinson＇s Disease induced by MPTP, which may be related to attenua- ting the degree of oxidative stress and improving the ability of resisting free radical injury.
出处
《卒中与神经疾病》
2012年第4期199-201,206,共4页
Stroke and Nervous Diseases
基金
湖北医药学院附属人民医院基金资助项目[No.(2006)163]
