原花青素抗小鼠实验性血管性痴呆的研究

目的研究原花青素的抗小鼠实验性血管性痴呆作用,探讨其保护作用机制。方法采用脑缺血再灌注合并尾静脉放血降压的方法制备小鼠血管性痴呆模型,小鼠分为假手术组、模型组、阳性对照组和原花青素低、中、高（50、100、200mg.kg-1）剂量组。小鼠水迷宫实验和避暗实验用于检测空间学习记忆行为。生化测量脑内超氧化物岐化酶,胆碱酯酶的活性和总抗氧化能力、及丙二醛含量。结果原花青素低、中、高3个剂量组均可减少水迷宫逃避潜伏期时间,增加穿台次数;可显著增加小鼠被动避暗潜伏期,减少避暗穿箱次数。提高小鼠脑组织超氧化物歧化酶活性,提高总抗氧化能力,降低脂质过氧化物含量,抑制胆碱酯酶的活性。结论原花青素有抗小鼠血管性痴呆的作用,它改善血管性痴呆的机制可能与抗氧化、抑制胆碱酯酶活性有关。

The Experimental Study of Procyanidine's Resist ance against Vascular Dementia of Mice

Aim To investigate procyanidine＇s protection against experimental vascular dementia of mice and to explore its mechanism. Methods The mice model of vascular dementia was induced by the method of cerebral ischemia/reperfusion and blood pressure reduction through tail bloodletting, Mice were randomly divided into 6 groups, including the sham-operated group, model group, positive control group, low-dose,middle -dose and high -dose procyanidine-treated group（50,100,200mg.kg^- 1 ）. The learning and memory abilities of mice were measured by water maze task and passive avoidance task. SOD and acetylcholinesterase （ACHE） activity, T-AOC and concentrations of MDA in the brain were determined by biochemistry method. Results Shortened mean escape latency and more frequent pass through the platform were detected in the procyanidine group than the model group in water maze task . Procyanidine treatment also significantly reversed the ischemia-induced retention deficit determined by a one trial step-down type of passive avoidance task. Procyanidine improved SOD activity and T-AOC, reduced acetylcholinesterase activity and concentration of lipid peroxidation. Conclusion Procyanidine has protective effects on experimental vascular dementia of mice. The may be＇mechanism related to anti-oxidation activity and inhibiting acetylcholinesterase activity.