葡萄内酯对脑缺血致血管性痴呆大鼠的保护作用

Protective effect of auraptene on cerebral ischemia-induced vascular dementia in rats

目的:考察葡萄内酯对脑缺血致血管性痴呆大鼠的保护作用。方法:SD大鼠随机分成假手术组、模型组、安理申组(1.028 mg.kg-1)和葡萄内酯低、中、高剂量(0.257,0.514,1.028 mg.kg-1)组,ig给药,连续52 d。采用永久性结扎大鼠双侧颈总动脉法建立血管性痴呆模型,以Morris水迷宫试验进行行为学测试,观察大鼠的学习记忆能力,检测大鼠脑组织中乙酰胆碱酯酶(AChE)和超氧化物歧化酶(SOD)的活性以及丙二醛(MDA)和谷氨酸含量的变化。结果:中、高剂量葡萄内酯可以明显缩短大鼠的逃避潜伏期,提高其穿越平台次数,增强大鼠的空间学习记忆能力,与模型组比较有极显著性差异(P<0.01)。葡萄内酯各剂量均能降低血管性痴呆大鼠AChE活性以及MDA和谷氨酸含量,与模型组相比,均有显著性差异(P<0.01)。葡萄内酯中、高剂量组的SOD活性明显低于模型组(P<0.01)。结论:葡萄内酯对血管性痴呆有保护作用,其作用机制可能与其降低MDA含量、乙酰胆碱酯酶活性以及谷氨酸对脑神经的毒害作用有关。

Objective： To investigate the protective effect of auraptene on cerebral ischemia-induced vascular dementia in Sprague-Dawley（SD） rats.Methods： SD rats were randomly divided into six groups,and orally administered with Aricept（1.028 mg·kg^-1,ig） and auraptene（0.257,0.514 and 1.028 mg·kg^-1,ig） for 52 days.Cerebral ischemia was induced by ligating the bilateral common carotid arteries.Spatial learning performance was evaluated by Morris water maze.The activities of acetylcholinesterase（AChE） and superoxide dismutase（SOD）,and the contents of malondialdehyde（MDA） and glutamic acid were assayed.Results： Auraptene at 0.514 and 1.028 mg·kg-1 significantly decreased the escape latency and the time spent in searching the target platform,strengthened the spatial learning memory（P〈0.01）.Compared with the ischemic control,auraptene at 3 doses significantly decreased AChE activity and the contents of MDA and glutamic acid（P〈0.01）.Auraptene at 0.514 and 1.028 mg·kg-1 significantly decreased SOD activity compared with ischemic control（P〈0.01）.Conclusion： Auraptene has a protective effect on cerebral ischemia-induced vascular dementia,which may result from decreasing the content of malondialdehyde,acetylcholinesterase activity and neuron toxicity of glutamic acid.