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目的:观察鹰嘴豆芽素A对β-淀粉样肽(Aβ25-35)致阿尔茨海默病(AD)模型小鼠学习记忆的影响,并对其作用机制进行初步探讨。方法:采用一次性侧脑室注射凝聚态Aβ25-35 3μg(1.0 mmol/L)方法制备痴呆模型。造模后,对照组和模型组灌胃等体积溶剂,给药组分别给予2 mg/kg和6 mg/kg鹰嘴豆芽素A,连续灌胃14天。通过Y-迷宫和跳台实验观察鹰嘴豆芽素A对痴呆小鼠学习记忆的影响;测定小鼠血清中丙二醛(MDA)含量和超氧化物歧化酶(SOD)的活性;常规HE染色观察小鼠海马形态学改变。结果:与对照组比较,模型组小鼠学习记忆功能明显减退,海马区神经细胞离散、固缩,排列不成行;鹰嘴豆芽素A治疗组能明显增强小鼠学习记忆能力,改善小鼠海马结构,降低痴呆小鼠血清MDA含量,增强SOD活性。结论:鹰嘴豆芽素A对Aβ25-35致AD模型小鼠记忆障碍有保护作用,其作用机制可能与其抗氧化作用有关。
OBJECTIVE: To observe the effects of chickpea sp A on the learning and memory of Alzheimer’s disease (AD) -induced model mice induced by β-amyloid peptide (Aβ25-35), and to explore its mechanism. Methods: The dementia model was prepared by intracerebroventricular injection of condensed Aβ25-35 3μg (1.0 mmol / L). After modeling, the rats in the control group and the model group were given the same volume of solvent by intragastric administration. The administration group was given 2 mg / kg and 6 mg / kg chickpea sp. A respectively for 14 days. The effects of chickpea splenicin A on the learning and memory abilities of mice with dementia were observed by Y-maze and step-down test. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) Morphological changes in hippocampus of mice. Results: Compared with the control group, the learning and memory abilities of the mice in the model group were significantly decreased, and the neurons in the hippocampus were discrete and contracted. The treatment with chickpea sp. A significantly increased the learning and memory ability and the hippocampus Structure, reduce the serum MDA content of dementia mice and enhance the activity of SOD. Conclusion: Chickpea sp. A has a protective effect on memory impairment induced by Aβ25-35 in AD mice, and its mechanism may be related to its antioxidative effect.