Effects Of Triptolide On Synaptophysin And Postsynaptic Density 95 In Hippocampus Of Chronic Cerebral Ischemia Model Rats

Objective:Chronic cerebral ischemia,which is always associated with the pathological process of Vascular dementia,Alzheimer disease,Binswanger disease and other kinds of cerebral vascular diseases, its clinical performance is mainly on cognitive dysfunction and neurological dysfunction. Its pathogenesis is very complex and the recent studies show that immune inflammation caused by CCI in the cognitive dysfunction plays an important role.Triptolide (TP) is a traditional anti-inflammatory medicine in China, it has the effect of anti-inflammatory and immunological suppression. And it had made a great curative effect on the immunological diseases such as rheumatoid arthritis and systemic lupus erythematosus. This experiment intends to examine the effect of TP on the expression of synaptophysin and postsynaptic density 95 in CCI model rats, and discuss the protection of TP to the CCI model rats' synaptic structure of the hippocampus from the angle of anti-inflammatory and the immuneregulation, will provide experimental basis for prevention and cure CCI clinically.Method:Take 30 healthy adult male SD rats and divide them into control, model and treatment groups randomly, each group of 10. Adopt double-side common carotid artery permanent ligation method (2-VO) to establish CCI model and treatment rats, and exposure the bilateral common carotid artery of the control group rats. The treatment group rats treated with intraperitoneal injection of TP solution 0.4 mg/kg·d for 28 days, the model group and control group rats treated with the same volume of 4% propanediol solution in the same way. Examine the form and number of each rat' hippocampus neuronal by toluidine blue dye's staining and use immunohistochemistry methods and RT-PCR method to detect the expressions of SYN and PSD-95 protein and mRNA in each rat' hippocampus.Results:1. Nebuchadnezzar toluidine blue dye show that the number and shape of cone layer neurons in the hippocampus CA1 area of the control group rats have no obvious change; the cells have a cone shape, regular arrangement and clear boundaries;the number of cone layer neurons in the hippocampus CA1 area of model group rats is significantly reduced compare the control group ones, intercellular space is increased and neurogliocyte is hyperplasia diffuse; the damage degree of cone layer neurons in the hippocampus CA1 area of the treatment group rats is less than the model group ones.2.The immunohistochemical stanining of the SYN shows that the SYN positive outcome'dying in the molecular layer of hippocampus CA1 area in the control group rats is deep and distribution uniformly; the quantity and average light density of SYN positive product in the hippocampus CA1 area molecular layer of the model group rats are obviously lower than the control group ones; the quantity and average light density of SYN positive product in the hippocampus CA1 area molecular layer of the treatment group rats are obviously higher than the model group ones.3.The immunohistochemical stanining of the PSD-95 finds that The PSD-95 positive cells in the hippocampus CA1 area cone layer of the control group rats are appear as a cone-shaped concentrated distribution, visible axons and dendritic sample swelled; the quantity and average light density of PSD-95 positive cells in the hippocampus CA1 area molecular layer of the model group rats are obviously lower than the control group ones; the quantity and average light density of PSD-95 positive cells in the hippocampus CA1 area molecular layer of the treatment group rats are obviously higher than the model group ones.4.RT-PCR displayed, the expression of SYN and PSD-95 mRNA in the model group rats'hippocampus is less than the control group rats. The expression of SYN and PSD-95 mRNA in the treatment group rats is increased compared with the model group rats.Conclusion:TP can promote the expressions of SYN and PSD-95'protein and mRNA in the hippocampus CA1 area; it also has a protection for hippocampus neuron of CCI model rats.