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目的:探讨黄芩茎叶总黄酮(SSTF)对大鼠双侧海马注射Aβ25-35引起的大鼠学习记忆功能和海马神经元形态变化的影响及机制。方法:将30只雄性Wistar大鼠随机分为对照组、模型组、总黄酮组,对照组及模型组灌胃纯化水,qd,d 8对照组海马注射生理盐水,继续灌胃;模型组双侧海马注射Aβ25-35(5μL),其他同对照组;给药组总黄酮(50 mg.kg-1,ig,qd),d8海马注射Aβ,继续灌胃,三组于d15采用Morris水迷宫实验观察大鼠学习记忆能力,测5 d,处死,硫堇Nissl染色观察海马神经元的变化,检测血清中丙二醛(MDA)含量。结果:模型组大鼠逃避潜伏期较对照组明显延长(P<0.05),给药组大鼠逃避潜伏期较模型组明显缩短(P<0.05);模型组海马CA1区局部神经细胞带脱失,脱失处胶质细胞增多,给药组细胞损伤较轻;模型组大鼠血清中MDA显著高于对照组(P<0.05),给药组血清中MDA明显低于模型组(P<0.05)。结论:黄芩茎叶总黄酮对海马注射Aβ25-35引起大鼠学习记忆能力降低及海马神经元形态变化具有保护作用,其机制可能是减少Aβ引起的脂质过氧化产物增多引起的氧化应激,并可对抗Aβ引起的胶质细胞增多。
AIM: To investigate the effects and mechanisms of total flavonoids (SSTF) from stems and leaves of Scutellaria baicalensis bauscht on learning and memory and the morphological changes of hippocampal neurons in rats induced by bilateral injection of Aβ25-35 into the hippocampus. Methods: Thirty male Wistar rats were randomly divided into control group, model group, total flavonoids group, control group and model group. Purified water was infused into the hippocampus of rats in the qd and d 8 groups, Aβ25-35 (5μL) was injected into the lateral hippocampus and the other rats were injected with Aβ (50 mg.kg-1, ig, qd) The learning and memory abilities of rats were observed and measured for 5 days. The rats were killed and the changes of neurons in hippocampus were observed by Nissl Nissl staining. The content of malondialdehyde (MDA) in serum was measured. Results: The escape latency in model group was significantly longer than that in control group (P <0.05), and the escape latency in treatment group was significantly shorter than that in model group (P <0.05). Local neuronal cells in hippocampal CA1 region of model group were lost, Compared with the control group, MDA in the model group was significantly higher than that in the control group (P <0.05). MDA in the serum of the treated group was significantly lower than that of the model group (P <0.05). Conclusion: The total flavonoids from stems and leaves of Scutellaria baicalensis Georgi can protect the hippocampus of rats from Aβ25-35-induced learning and memory impairment and morphological changes of hippocampal neurons. The mechanism may be to reduce the oxidative stress induced by Aβ-induced increase of lipid peroxidation products, And against Aβ induced glial cells increased.