The Basic Study On The Effect Of Injection Of Puerarin And Gastrodine On Experimental Mouse Model Of Parkinson's Disease

Objective:To study the possible mechanism of the injection of gastrodine and puerarin (IGP) in the treatment of Parkinson's desease (PD).Methord:C57BL/6 mice were divided randomly into four group:control group,model group,IGP group and Madopar group. Mice in the model group,IGP group and Madopar group were injected with MPTP to establish PD animal model and then were treated with normal saline(NS), IGP and Madopar respectively. Animals were examined behaviorally with the pole test and the traction test. After the animals were killed, the expression of Bcl-2 and Bax in the substantia nigra (SN) of mice were examined. At the same time the morphology of neurons in the SN was observed with microscope.Result:1. Dopaminergic neuron in the model group has irregular shape (polygon or long spindle) and unclear structure; The number of neurons in the model group decreased remarkably; The number of neurons in the IGP group and the Madopar group was close to the number in the control group.2. The time of the pole test in the model group on the seventh,the fourteenth and the twenty-first day were prolonged remarkably compared with the normal group (P<0.01,P<0.01,P<0.05); The time of the pole test in the IGP group on the fourteenth and the twenty-first day increased remarkably, compared with the model group (P<0.05,P<0.05); The time of the pole test in the Madopar group on the fourteenth and the twenty-first day increased remarkably, compared with the model group (P<0.05,P<0.05); The time of the pole test in the IGP group and Madopar group has little difference(P>0.05,P>0.05).3. The scores of the traction test in the model group on the seventh,the fourteenth and the twenty-first day were decreased remarkably compared with the normal group (P<0.01,P<0.05,P<0.01); The scores of the traction test in the IGP group on the fourteenth and the twenty-first day increased remarkably, compared with the model group (P<0.01,P<0.01); The scores of the traction test in the Madopar group on the fourteenth and the twenty-first day increased remarkably, compared with the model group (P<0.05,P<0.01); The scores of the traction test in the IGP group and Madopar group have little difference (P>0.05,P>0.05).4. The number of Bcl-2 positive neurons in the SN of mice in the model group decreased remarkably compared with the normal group (P<0.01); When treated with IGP and Madopar, the number of Bcl-2 positive neurons increased remarkably compared with the model group (P<0.01,P<0.01); The number of Bcl-2 positive neurons in the IGP group and Madopar group has little difference(P>0.05).5. The numbers of Bax positive neurons in the SN of mice in the model group increased remarkably compared with the normal group(P<0.01); When treated with IGP and Madopar, the numbers of Bax positive neurons decreased remarkably compared with the model group(P<0.01,P<0.01); The number of Bax positive neurons in the IGP group and Madopar group has little difference(P>0.05).Conclusions:1. IGP could improve the dyskinesia of PD mouse model.2. IGP could repaire the damage of dopaminergic neurons in the SN of PD mouse model.3. IGP has the same therapic effect on PD as Madopar.4. IGP's therapic effect on PD might be mediated by the anti-apoptotic process.