摘要
目的探讨壳聚糖磷脂酰胆碱对海马注射Aβ25-35所致阿尔茨海默病(AD)模型大鼠脑内蛋白激酶C-δ(PKC-δ)、钙结合蛋白(Iba1)表达的影响。方法随机将50只Wistar大鼠分为对照组,AD模型组,壳聚糖磷脂酰胆碱低、中、高剂量组,每组10只。除对照组外,其余各组大鼠双侧海马CA1区各一次性注射凝聚态2.5μLAβ25-355μg/μL制备AD模型,用Morris水迷宫检测大鼠学习记忆能力,用免疫组织化学方法检测大鼠脑内PKC-δ、Iba1的表达。结果壳聚糖磷脂酰胆碱明显缩短Aβ25-35所致AD模型大鼠的潜伏期,增加穿越平台的次数,显著降低PKC-δ、Iba1的阳性表达。结论壳聚糖磷脂酰胆碱通过下调脑组织PKC-δ表达,抑制小胶质细胞增生和激活,减轻脑皮层和海马神经元炎性反应,对Aβ25-35所致AD模型大鼠学习记忆障碍具有明显的改善作用。
Objective To investigate the effect of chitosan phosphatidyl choline on the expressions of protein kinase C-δ(PKC-δ) and calcium binding protein( Ibal ) in AD rats brain induced by Aβ25-35. Methods Fifty wistar rats were randomly divided into five groups: the control group, the AD model group ,the chitosan phosphatidyl choline low-dose group, the medium-dose group and the high-dose group. Two point five microliter of Aβ25-35 (5μg/μL) was injected into the CA1 area of the rat hippocampus to establish the AD model. The rat learning and memory abilities were tested through the method of Morris water maze. The expressions of PKC-δ and Ibal in hippocampus and cerebral cortex were detected with the immunohistochemical method. Results Chitosan phosphatidyl choline could obviously shorten the AD rats latency caused by Aβ25_35, increase the times of passing through platform, and significantly reduce the PKC-δ and Ibal positive expressions in AD hippocampus and cerebral cortex of rats. Conclusion Chitosan phosphatidyl cho- line can improve the learning and memory abilities of AD rats caused by Aβ25-35, depress the proliferation and activation of microglia in the rat brain, lessen inflammation response , and contribute to neuroprotection and anti-dementia through down-regulating the PKC-δ expression.
出处
《山东大学学报(医学版)》
CAS
北大核心
2012年第10期37-40,45,共5页
Journal of Shandong University:Health Sciences
基金
山东省自然科学基金(y2008c125)