Effect Of Polygonum Saponins On Learning And Memory Of Rats With Parkinson's Disease And Its Mechanism Of Action

Backgroud:Parkinson’s disease is a common clinical degenerative disease of the central nervous system.The clinical symptoms are complicated,including typical movement symptoms and complex non-motor symptoms,which can cause a great burden to patients and their families.With the increasing incidence of the disease,prevention and control of Parkinson’s disease has become an important subject of medical research.Polygoni multiflori has the effect of tonify the liver and kidney and nourish the Bone marrow.It is often used in the neurodegenerative diseases and adopted by many doctors in the treatment of Parkinson’s disease.The PD rat model induced by rotenone(RT)was used as the research object.The behavioral test,biochemical method and immunohisto-chemical staining method were used to observe the main active ingredient of 2,3,5,4 ’tetrahydroxy-stilbene glucoside,and its effect on the behavior and learning memory of rats with Parkinson’s disease.In this way,the possible mechanism of using polygoni multiflori to control PD was investigated to provide basic support in this area,which is of great significance for the better development and dissemination of Chinese medicine.Objective:1.To explore the effect of TSG on the behavior and learning memory of PD rats.2.To investigate the effect of TSG on the level of oxidative stress in the brain of PD rats.3.The effects of TSG on the expression of brain derived neurotrophic factor and tyrosine kinase B signaling pathway in hippocampus of PD rats were studied and the mechanism of TSG on the prevention and treatment of PD was further elaborated.Methods:1.A model was established by subcutaneously injecting rotenone into the neck and back of Lewis rats for 8 weeks,and TSG was administered by gavage.2.Animals were randomly divided into 4 groups,10 in each group,which were the normal group(injected of sunflower oil,distilled water gavage),the model group(injected sunflower oil emulsified rotenone,distilled water gavage),TSG administration group(injected sunflower oil emulsified rotenone,TSG low-dose group 30mg/kg,TSG high-dose group 60mg/kg).3.The animal behavior was scored every week.The learning and memory of the animals were detected by object recognition experiment.Cortical oxidative stress of rats was detected by biochemical method.The expression of the brain derived neurotrophic factor and its receptor TrkB in the hippocampus of rats was detected by immunohisto-chemistry.Results:The behavioral score of the rats in the control group was always 0,and the behavioral score of the model group increased significantly with the prolongation of the modeling time.After 4 weeks of modeling,the behavioral score of TSG high-dose group was significantly lower than that of the model group(p<0.05).At the 6th week of modeling,the behavioral scores of the 2-dose rats in the TSG group were significantly lower than those in the model group(p<0.05).In the object recognition experiment,the recognition index of the model group was lower than the normal group,and the recognition index of TSG group increased.There was no significant difference in the content of MDA in the cortex of each group.Compared with normal group,the activity of GSH and SOD in the cortex of model rats increased significantly(p<0.05).Compared with the model group,the SOD activity of TSG in high-dose group decreased significantly(p<0.05).The number of BDNF positive cells,dyed area and mean light density in the hippocampus CA1 area of the model group decreased significantly(p<0.05)compared with the normal group(p<0.05).The number of TrkB positive cells and the stained area were significantly decreased compared with the normal group(p<0.05).TSG administration significantly increased the expression of BDNF and TrkB in hippocampal CA1 area(p<0.05).Conclusions:1.TSG has a better effect on motor symptoms of PD.2.TSG can improve the level of oxidative stress in the brain of animal models,and play a certain role in the prevention and treatment of PD.3.TSG can improve and delay the progression of PD motor symptoms and cognitive decline by increasing the expression of brain-derived neurotrophic factor and its receptor in the hippocampus of model animals.