人参皂苷Re对帕金森病小鼠保护作用——人参皂甙Re抗黑质神经元凋亡的机制初探

The Protective Effects of Ginsenoside Re from Mptp-Induced Parkinson's Disease C57BL Mice —— Possible Mechanisms of the Protective Effects of Ginsenoside Re on Apoptosis in Substantia Nigra Neurons

目的 :研究人参皂苷Re对 1 甲基 4 苯基 1,2 ,3,6 四氢吡啶 ( 1 methy 4 phenyl 1,2 ,3,6 tetrahy dropyridine ,MPTP)诱致C5 7BL小鼠黑质神经元凋亡的保护作用及其可能机制。方法 :用MPTP皮下注射C5 7BL小鼠制备帕金森病 (Parkinson’sdisease ,PD)模型 ,灌胃给予人参皂苷Re预处理后 ,用TH组织化学染色 ,TUNEL染色观察黑质神经元的变化及凋亡情况 ;免疫组织化学检测Bcl 2 ,Bax蛋白表达。结果 :13mg·kg-1,2 6mg·kg-1人参皂苷Re预处理能使黑质致密带 (SNc)部位的TH染色阳性神经元增多 ,TUNEL染色阳性率降低 ,以及Bcl 2蛋白表达增加 ,Bax蛋白表达减少。结论 :人参皂苷Re对MPTP诱致小鼠黑质神经元凋亡有明显的保护作用 ;Bcl 2表达的升高和Bax表达的降低可能是人参皂苷Re抗凋亡的重要机制。

AIM:To investigate the role of ginsenoside Re in preventing from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced apoptosis of the substantia nigra neurons in the mouse model of Parkinson's disease (PD). METHOD: C57BL mice were administrated sc. with MPTP to establish PD model. The pretreatment groups were given different doses of ginsenoside Re (13,26 mg·kg -1) ig. for 13d. Tyrosine hydroxythase (TH) immunostaining and TDT-mediated dUTP nick-end labeling(TUNEL) staining were used to observe the damage of substantia nigral neurons. To detect the expression of Bcl-2,Bax protein the immunohistochemistry was explred.RESULT:Pretreatment with gisenoside Re (13,26 mg·kg -1) was shown to increase TH-positive neurons and decrease the TUNEL-positive ratio.Futhermore,Ginsenoside Re could enhance the expression level of Bcl-2 protein and reduce the expression level of Bax protein. CONCLUSION:Ginsenoside Re showed protective effects on MPTP-induced apoptosis in the PD model mouse nigral neurons and this effect may be attributable to increasing the expression level of Bcl-2 and decreasing the expression level of Bax.