摘要
目的通过对帕金森病(PD)大鼠模型中脑黑质部位氧化应激反应的观察,探讨PD发病的可能机制。方法16只健康雄性SD大鼠随机分为PD组和对照组。应用立体定向技术建立6-羟基多巴胺(6-OHDA)毁损的PD模型,通过多巴胺受体激动剂阿朴吗啡(APO)测试大鼠旋转行为。化学比色法分别测定中脑黑质部位超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活性及丙二醛(MDA)含量。结果PD组大鼠黑质部位GSH-PX、SOD活性较对照组明显下降,具有显著性差异(P<0.05);MDA含量较对照组明显升高,具有显著性差异(P<0.05)。结论中脑黑质部位氧化应激反应增强及抗氧化保护机制减弱可能是引起PD发病的重要机制之一。
Objective By studying the oxidative stress of the substantia nigra in experimental Parkinson's rats, to explore the pathogenesis of Parkinson's disease (PD) . Methods Sixteen male Sprague - Dawley rats were randomly divided into normal saline (NS) group and PD group. Hemi - Parkinsonism rat model was established by stereotaxic 6 - OHDA lesions in substantia nigra, with apomorphin (Apo) - induced rotational behavior conducted to assay the quality of the model. Spectropho-tometry was employed to determine the activities of superoxide dismutase (SOD) and gluathione peroxidase (GSH - PX) and the content of malondialdehyde (MDA) in substantia nigra. Results The activities of SOD and GSH- PX were much lower, and the content of MDA was much higher in PD group than in NS group ( P < 0.05) . Conclusion The enhanced oxidative stress and decreased antioxidation abilities in substantia nigra may be one of the important mechanisms of PD.
出处
《徐州医学院学报》
CAS
2004年第6期519-521,共3页
Acta Academiae Medicinae Xuzhou
