百草枯对小鼠黑质多巴胺能神经元氧化应激的影响

目的探讨百草枯干预对小鼠黑质氧化应激的影响。方法用口服百草枯的途径,建立小鼠帕金森病(PD)模型。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)水平的变化;同时采用免疫组化ABC法观察黑质部位酪氨酸羟化酶(TH)阳性表达神经元。结果口服百草枯两月后,黑质的SOD和GSH-PX的活性较对照组明显下降,MDA水平明显升高,与正常对照组相比有显著性差异(P<0.05);小鼠黑质部TH阳性细胞明显减少(P<0.01)。结论百草枯可造成小鼠PD样的行为表现;小鼠黑质部SOD和GSH-PX的活性降低,MDA浓度增高,提示氧化应激参与了百草枯所致PD的发病机制。

Influence of paraquat on oxidative stress of dopaminergic neuron in substantia nigra of mice

Objective To explore the oxidative stress pathogenesis of Parkinson's disease(PD) induced by paraquat in substantia nigra of mice. Methods The model of PD was established by oral administration of paraquat to mice.The spectrophotometry was used to determine the activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-PX) and the content of malondialdehyde(MDA) in substantia nigra.At the same time,number of tyrosine hydroxylase(TH) positive neurons in substantia nigra of mice was estimated by immunohistochemistry. Results The activities of SOD and GSH-PX were significantly decreased,and the content of MDA was increased in paraquat-treated mice compared to that of mice treated by saline taken orally(P<0.05).Number of TH positive neurons in substantia nigra of mice was also significantly decreased(P<0.01). Conclusion Paraquat can induce mice to appear a series of behaviors that are similar to PD.The decreased activities of SOD and GSH-PX,and increased content of MDA in substantia nigra of mice indicate that oxidative stress may be involved in the pathogenic mechanism of PD induced by paraquat.