ObjectiveTo investigate the effect of Ligustrazine on whether the activation of Wnt signal pathway of Alzheimer's disease(AD) rat brain inflammatory tissue,and to explore its action mechanism.MethodsUsing the beta amyloid peptide 25-35(A 25-35)of model rats with Alzheimer disease made bilateral hippocampal injection,observe the effects of Ligustrazine on tau protein in hippocampus of AD rats on the part of the phosphorylation site and amyloid beta(A beta)effects of APP precursor levels in the Wnt pathway,beta catenin(Beta -catenin)and glycogen synthase kinase 3 beta(GSK-3 beta)level,at the same time,use immune group to determination of 4 groups of AD rats hippocampal A deposition of the degree of technology.ResultsThis study showed that the model of unilateral cerebral cortex in rats of A group were obviously visible beta, intercellular space mirror under brown change. And the intervention of Ligustrazine,brown component is gradually reduced,ligustrazine can inhibit A deposition,significantly inhibited the phosphorylation of tau,inhibiting the activity of GSK-3,reduce the beta -catenin degradation. ConclusionTMP reduces the beta -catenin degradation,thus preventing tau protein phosphorylation through the inhibition of hippocampus GSK-3 expressionin AD rat,and can activate Wnt pathway to inhibit the A beta protein induced neurotoxicity,which playsa role in nerve cell protection.%目的：探讨川芎嗪是否能通过激活Wnt信号通路改善阿尔茨海默病（AD）大鼠脑组织炎性，并探讨其作用机制。方法采用β淀粉样肽25-35（Aβ25-35）双侧海马注射造阿尔茨海默病大鼠模型，观察川芎嗪对AD大鼠海马tau蛋白上部分磷酸化位点及β淀粉样蛋白（Aβ）前体APP水平的影响，Wnt途径中β-联蛋白（β-catenin）和糖原合成激酶3β（GSK-3β）水平，同时采用免疫组化技术测定4组AD大鼠海马Aβ沉积程度。结果模型组大鼠单侧大脑皮质区Aβ沉积明显，镜下可见细胞间隙呈褐色改变。而经川芎嗪干预后，褐色成分逐渐减少，川芎嗪可显著抑制Aβ沉积，显著抑制tau磷酸化，抑制GSK-3活性，减少β-catenin降解。结论 TMP通过对AD大鼠海马组织GSK-3β阳性表达的抑制、导致β-catenin降解下降，从而抑制tau蛋白过度磷酸化，并可激活Wnt信号通路抑制Aβ蛋白引起神经毒性，从而发挥神经细胞保护作用。
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