天丝饮对Aβ25-35所致阿尔茨海默病模型大鼠的影响

Impacts of Tiansi Liquid on Alzheimer's Disease Induced by Aβ25-35 in the Model Rats

目的研究天丝饮对侧脑室注射β-淀粉样蛋白(Aβ25-35)致阿尔茨海默病(AD)模型大鼠相关病理变化的作用。方法将40只大鼠随机分为正常组、假手术组、模型组、天丝饮组,每组10只。采用单侧侧脑室注射Aβ25-35建立AD大鼠模型,Morris水迷宫检测各组大鼠空间学习记忆能力、苏木精-伊红(H-E)染色法观察各组海马神经元形态、比色法测量各组大鼠脑组织中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量。结果与空白组、假手术组比较,模型组大鼠学习记忆能力明显减退(P<0.01),脑组织中SOD活力显著降低(P<0.01),MDA含量明显升高(P<0.01);与模型组比较,天丝饮组学习记忆能力得到明显改善(P<0.01),脑组织中SOD活力显著升高(P<0.01)、MDA含量明显降低(P<0.01)。结论天丝饮对Aβ25-35诱导的AD模型大鼠的空间学习记忆障碍及神经元损伤均具有显著改善作用,其作用可能与其具有抗自由基,保护、营养神经元,抑制脑组织损伤有关。

Objective To study the impacts of Tiansi Liquid on the relevant pathological changes in Alzeimer＇s disease（AD） model rats induced by the injection of Aβ25 -35 in lateral ventricle. Methods Forty rats were randomized into a normal group, a sham - operation group, a model group and a Tiansi Liquid group, 10 rats in each one. Injection of Aβ25 -35 in lateral ventricle was used to establish AD rat models. Morris water puzzle test was adopted to determine the spatial learning and memory ability of rats in each group. HE staining was used to observe the morphology of hippoeampal neurons. Colorimetrie method was ap- plied to determine the activity of SOD and MDA content in brain tissue of rat. Results Compared with the blank group and the sham - operation group, the learning and memory ability of rats was reduced obviously in the model group（P 〈 0.01 ）, SOD activity was declinedsignifieantly （P 〈 0.01 ）and MDA content was in- creased apparently （ P 〈 0.01 ）. Compared with the model group, the learning and memory ability was im- proved apparently in the Tiansi Liquid group（ P 〈 0.01 ）, SOD activity in brain tissue was increased signifi- cantly and MDA content was reduced apparently （ P 〈 0.01 ）. Conclusion Tiansi Liquid improves signifi- cantly in the disorders of the spatial learning and memory ability and neuronal damage in AD model rats in- duced byAβ25 -35. The effect is probably related to its resistance to free radicals, theproteetion and nutrition of neurons, as well as the inhibition of brain tissue damage.