首页> 中文期刊>郑州大学学报(医学版) >人参皂苷 Rg1对帕金森病小鼠黑质多巴胺能神经元凋亡及EphB1、TH、P-c-Jun蛋白表达的影响

人参皂苷 Rg1对帕金森病小鼠黑质多巴胺能神经元凋亡及EphB1、TH、P-c-Jun蛋白表达的影响

     

摘要

目的:观察人参皂苷Rg1对MPTP所致帕金森病( PD)模型小鼠黑质多巴胺能神经元凋亡及酪氨酸羟化酶(TH)、EphB1和P-c-Jun蛋白表达的影响。方法:将27只C57BL/6小鼠等分为对照组、模型组和人参皂苷Rg1组。腹腔注射人参皂苷Rg1预防给药3 d,腹腔注射MPTP构建PD模型。观察不同时间点小鼠游泳情况。 MPTP给药2周后采用TUNEL染色检测小鼠黑质多巴胺能神经元凋亡情况,采用免疫组化检测黑质EphB1蛋白的表达,采用Western blot检测黑质TH、P-c-Jun蛋白的表达。结果:模型组小鼠不同时间点游泳实验分值低于对照组和人参皂苷Rg1组(P均<0.05)。模型组黑质多巴胺能神经元凋亡数、EphB1阳性细胞数和P-c-Jun蛋白相对表达量均高于对照组和人参皂苷Rg1组,而模型组黑质TH蛋白相对表达量低于对照组和人参皂苷Rg1组(P均<0.05)。结论:人参皂苷Rg1可能通过减少黑质多巴胺能神经元凋亡以及降低EphB1、P-c-Jun的表达而改善PD的症状。%Aim:To explore the influence of ginsenoside Rg 1 on apoptosis of dopamine neurons , expressions of TH , EphB1 and P-c-Jun proteins in substantia nigra of mice with Parkinson′s disease ( PD ) induced by MPTP .Methods:Twenty-seven C57BL/6 mice were randomly divided into control group , model group and ginsenoside Rg1 group.The mice of ginsenoside Rg1 group were pretreated with ginsenoside Rg 1.MPTP was injected intraperitoneally to mice to make PD model.The swimming test of mice was determined at different time points .Two weeks later, apoptosis of dopamine neurons in substantia nigra of the mice was determined by TUNEL staining .The expression of EphB 1 protein in substantia nigra of the mice was detected by immunohistochemistry .The expressions of TH and P-c-Jun proteins in substantia nigra of the mice were detected by Western blot .Results:The swim-score values of model group were significantly lower than those of con-trol group and ginsenoside Rg1 group at different time points(P<0.05).The number of apoptosis dopamine neurons , the positive expression of EphB 1 protein, and the relative expression of P-c-Jun protein of the model group were higher than those of control group and ginsenoside Rg1 group(P<0.05).The relative expression of TH of model group was significant-ly lower than those of the control group and ginsenoside Rg 1 group(P<0.05).Conclusion:Ginsenoside Rg1 may improve the symptoms of PD through decreasing apoptosis of dopamine neurons , and reducing the expressions of EphB 1 and P-c-Jun.

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