人参皂苷Rg1对MPTP致帕金森病模型小鼠多巴胺能神经元保护作用研究

目的研究人参皂苷Rg1（GinsenosideRg1，Rg1）对1-甲基4-苯基-1，2，3，6-四氢吡啶（1-methy-4-phenyl-1，2，3，6-tetra—hydropyrldine，MPTP）致帕金森病小鼠黑质（substantla nigra，SN）多巴胺（dopamine，DA）能神经元变性的保护作用及其可能机制。方法C57BL6小鼠随机分为对照组（NS，ip）、MPTP组（30mg·kg^-1×5d，ip）及Rg，（5mg·kg^-1×8d，ip）预处理组。应用逆转录-聚合酶链式反应（RT—PCR）、免疫组织化学染色等技术观察了SN Caspase-3mRNA、Bcl-2 mRNA、Bax mRNA、酪氨酸羟化酶（tyrosine hydroxylase，TH）mRNA的表达水平和黑质致密带（substantia nigra zona compacta，SNzc）TH免疫反应阳性细胞数量等多项指标的变化，用高效液相色谱法检测小鼠纹状体（stfiatum，Str）内DA及其代谢物二羟基苯乙酸（dihydroxyphenylaceti cacid，DOPAC）和高香草酸（homovanillic acid，HVA）含量。结果MPTP组SN内TH阳性细胞数量、Str内DA及其代谢产物DOPAC和HVA的含量明显减少，应用Rg1后可逆转上述改变（P〈0．01）。MPTP组SN Bcl-2、THmRNA的表达明显降低（P〈0．01）；Caspase-3、Bax mRNA的表达明显增加（P〈0．01）。应用Rg1后可逆转上述改变（P〈0．05）。结论Rg1对MPTP致帕金森病小鼠SNDA能神经元具有明显的保护作用，其机制可能与抗凋亡过程有关。

Neuroprotective Effects of Ginsenoside Rg1 on the Dopaminergic Neurons in the Substantia Nigrain Mptp-Treated C57BL6 Mice

Aim To investigate whether ginsenoside Rgl can prevent the degeneration of dopamincrgic neurons in the substantia nigra （ SN ） in 1 -methy-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP） treated C57 BL6 mice. Method Mice were randomly divided into three groups： control group （NS, ip）, MPTP group （30mg·kg^-1× 5d, ip） and Rgl （ 5mg.kg^-1 × 8d, ip） pretreatment group. Using RT-PCR, tyrosine hydroxylase （ TH ） immunohistochcmistry and HPLC,the degeneration of dopaminergic neurons was measured in the SN of MPTP treated mice and assessed the effects of treatment with ginsenoside Rgt. Results The number of TH-immunoreactive cells in the SN of MPTP treated mice, as well as the contents of dopamine and its metabolites in the striatum, decreased significantly. Treatment with ginscnoside RgI reversed these effects（ P 〈0.01 ）. The expression of Bcl-2 and TH mRNA in the SN also decreased significantly in MPTP treated mice （ P 〈 0.01 ）, while the expression of Caspase-3 and Bax mRNA increased significantly（ P 〈0.01 ）. Treatment with ginsenoside Rgl reversed the above changes（ P 〈0.05）. Conclusion Ginsenoside Rgl is neuroprotective against the neurotoxin MPTP, possibly due to its anti-apoptosis activity.