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脂联素干预改善血管性痴呆大鼠认知功能的作用研究 被引量:3

Effect of Adiponectin Intervention on Cognitive Function in Rats with Vascular Dementia
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摘要 目的:探讨血管性痴呆(VD)大鼠脑组织脂联素(APN)水平变化及其与脑微血管新生和认知功能的关系。方法:45只SD大鼠随机分为假手术组、模型组和APN组,各15只。模型组采用手术永久结扎大鼠双侧颈总动脉的方法制备VD模型,APN组在造模后将携带APN基因的慢病毒载体注入大鼠尾静脉。干预后8周,采用Morris水迷宫检测大鼠的认知功能,免疫组织化学法测定脑组织APN、血管内皮细胞生长因子(VEGF)和CD31的表达水平。结果:与假手术组相比,模型组大鼠逃避潜伏期延长,目标象限停留的时间百分比缩短,脑组织APN表达水平下降,VEGF及CD31表达水平增加,差异均有统计学意义(P<0.05)。与模型组比较,APN组大鼠逃避潜伏期降低,目标象限停留时间百分比增加,大鼠脑组织APN、VEGF及CD31表达水平增加,差异均有统计学意义(P<0.05)。结论:APN干预有利于改善VD大鼠的认知功能,可能与增加脑白质血管形成有关。 Objective: To investigate the changes of adiponectin (APN) levels in brain tissue of rats with vascular dementia (VD), and its role with brain angiogenesis and cognitive function. Methods: VD model was pre- pared by permanent bilateral carotid artery ligation (2VO). The lentiviral vectors encoding APN gene was injected into rat's tail vein for APN intervention. Forty-five SD rats were randomly divided into sham group (sham-op-erated, n=15), VD group (2VO, n=15) and APN group (2VO+APN, n=15). The cognitive function of rats was re- corded by Morris water maze. The expressions ofAPN, VEGF and CD31 protein were determined by immtmo-histochemistry. Results: Compared with those in sham group, the escape latency was prolonged and the percentage of time spending in the goal quadrant was shortened in VD group; the expression of APN protein in brain tissue decreased but the expressions of VEGF and CD31 protein in brain tissue increased (P〈0.05). Compared with those in VD group, APN intervention significantly reduced the escape latency and prolonged the percentage of time spending in the goal quadrant in APN group, and the expressions ofAPN, VEGF and CD31 proteins in brain tissue increased (P〈0.05). Conclusion: APN intervention can improve the cognitive function of rats with VD, which may be related to the increase of angiogenesis in white matter.
出处 《神经损伤与功能重建》 2017年第6期479-482,共4页 Neural Injury and Functional Reconstruction
基金 湖北省卫计委项目(No.WJ2015MB101)
关键词 脂联素 血管性痴呆 认知障碍 血管内皮生长因子类 大鼠 adiponectin vascular dementia cognitive impairment vascular endothelial growth factors rats
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