论文部分内容阅读
目的探讨黄芪多糖(Astragalus polysaccharide,APS)对大鼠阿尔茨海默病(Alzheimer’s disease,AD)模型大鼠的疗效及其作用机制。方法将48只SPF大鼠随机分成3组,每组各16只:对照组、模型组和治疗组;模型组和APS治疗组采用Aβ25-35(80 pmol/μL)双侧脑室注射大鼠诱导AD模型,模型制备成功后APS治疗组给予APS(400 mg/kg)灌胃,1次/d,连续60 d;对照组和模型组给予等剂量生理盐水灌胃,1次/d,连续60 d;治疗结束后采用水迷宫实验(MWM)评价各组大鼠定位航行能力和记忆能力;MWM实验结束后处死各组大鼠获取海马行常规HE染色观察病理组织学变化,行Western-blot检测海马组织中淀粉样蛋白(amyloid peptide protein,APP)、β-淀粉样蛋白(amyloid peptide-β,Aβ)、磷酸化微管相关蛋白(Phosphorylation tau,p-tau)、糖原合成酶激酶3β(glycogen synthase kinase 3beta,GSK3)和蛋白磷酸酯酶2A(protein phosphatase2A,PP2A)等蛋白的表达水平。结果与模型组相比,APS治疗组可显著改善大鼠的定位航行能力(P<0.01)与学习记忆能力(P<0.01);HE染色表明APS治疗组可修复Aβ25-35所致的大鼠海马损伤;Western-blot表明与模型组相比,ASP治疗组APP,Aβ,p-tau,GSK3β和BACE1的蛋白水平下调(P<0.05,P<0.01,P<0.01,P<0.05,P<0.01),PP2A的蛋白水平上调(P<0.05)。结论 APS对Aβ25-35所致的AD具有保护作用。
Objective To investigate the curative effect and mechanism of Astragalus polysaccharide (APS) on Alzheimer’s disease (AD) model rats. Methods Forty-eight SPF rats were randomly divided into three groups of 16 rats in each group: control group, model group and treatment group. Aβ25-35 (80 pmol / μL) AD model, the APS treatment group was given APS (400 mg / kg) once a day for 60 days after the successful preparation of the model. The rats in the control group and model group were given gavage once a day for 60 days d. The water maze test (MWM) was used to evaluate the positioning ability and memory ability of rats in each group. After the MWM experiment, the rats in each group were sacrificed and the hippocampus was harvested for histopathological changes by routine HE staining. In the hippocampus tissue, amyloid peptide protein (APP), amyloid peptide-β (Aβ), phosphorylation tau (p-tau), glycogen synthase kinase 3β glycogen synthase kinase 3beta, GSK3) and protein phosphatase 2A (PP2A). Results Compared with model group, APS treatment group could significantly improve the navigation ability (P <0.01) and learning and memory ability (P <0.01). HE staining showed that APS treatment group could repair Aβ25-35-induced rats The protein level of APP, Aβ, p-tau, GSK3β and BACE1 in ASP group was significantly lower than that in model group by Western-blot (P <0.05, P <0.01, P < 0.01), and the protein level of PP2A was up-regulated (P <0.05). Conclusion APS can protect AD induced by Aβ25-35.