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目的观察降血脂药普伐他汀对慢性脑缺血大鼠的β淀粉样蛋白(Aβ)水平的影响。方法39只雄性SD大鼠分为正常饮食组(6只),高脂饮食组随机分为空白对照组(7只)、普伐他汀服用组(7只)、单纯脑缺血组(9只)及普伐他汀加脑缺血组(10只),采用结扎双侧颈总动脉建立CVI模型,于术后1个月行为学试验后,测血脂及Aβ水平。取脑组织,行病理学分析及ELISA检测Aβ水平。结果未治疗组(空白对照、单纯脑缺血组)血脂水平升高,但无显著差异(p>0.05),治疗组为正常水平。与正常饮食组相比,其余各组均无明显运动功能障碍,第4周平台定位时间、搜索策略无显著性差异(p>0.05)。脑病理学呈慢性缺血性改变结构欠清晰,神经元固缩或均匀着色,但明显的细胞坏死改变较少见;白质疏松明显。ELISA显示单纯缺血组Aβ较对照组明显升高,而治疗组Aβ下降至略高于对照组水平。结论普伐他汀能够降低脑内Aβ水平,这种降脂外的调节Aβ代谢作用提示血脂代谢异常参与了AD发病。
Objective To observe the effect of hypolipidemic pravastatin on amyloid beta (Aβ) in rats with chronic cerebral ischemia. Methods Thirty-nine male Sprague-Dawley rats were randomly divided into normal diet group (n = 6), high fat diet group (n = 7), pravastatin treatment group (n = 7), cerebral ischemia group ) And pravastatin plus cerebral ischemia group (10). CVI model was established by ligation of bilateral common carotid arteries, and blood lipid and Aβ levels were measured at 1 month after the behavioral test. Take brain tissue, pathological analysis and ELISA detection of Aβ levels. Results In the untreated group (blank control, simple cerebral ischemia group), the level of blood lipid increased but there was no significant difference (p> 0.05). The treatment group was normal. Compared with the normal diet group, there was no significant motor dysfunction in the other groups. There was no significant difference in the positioning time and search strategy in the fourth week (p> 0.05). Cerebral pathology showed chronic ischemic changes in the structure is not clear, neuronal shrinkage or uniform coloring, but the obvious changes in cell necrosis is rare; obvious white matter loosening. ELISA showed that Aβ was significantly increased in the ischemia group compared with the control group, while Aβ in the treatment group was slightly lower than that in the control group. Conclusions Pravastatin can reduce the level of Aβ in the brain. The regulation of Aβ metabolism besides lipid lowering suggests that dyslipidemia is involved in the pathogenesis of AD.