中文摘要：

目的探讨丹溪痛风方（DGP）对阿尔茨海默病（AD）小鼠海马的影响。方法 C57BL/6小鼠随机分成对照组,模型组,治疗组（吡拉西坦0.42 g/kg）,DGP高、中、低剂量组（DGP 52,26,13 g/kg）。采用小鼠双侧海马微量注射（10μg）β-淀粉样蛋白1-42（Aβ1-422 g/L）和腹腔注射D-半乳糖（180 mg/kg）诱导AD小鼠。给予小鼠连续治疗35 d后处死取材。采用Morris水迷宫测试小鼠学习记忆能力,观察小鼠海马结构,采用双抗体夹心法测定海马β-淀粉样蛋白前体蛋白（APP）、Aβ1-42、白介素（IL）-1β和肿瘤坏死因子（TNF）-α水平。结果与对照组比较,模型组小鼠海马潜伏期和游泳距离明显增加（P〈0.05）,海马目标停留时间和跨平台次数明显减少（P〈0.05）,海马APP、Aβ1-42、IL-1β和TNF-α水平明显升高（P〈0.05）;与模型组比较,DGP高、中剂量组AD小鼠海马学习记忆能力明显改善（P〈0.05）,海马神经元结构明显改善,海马APP、Aβ1-42、IL-1β和TNF-α水平明显降低（P〈0.05）。结论 DGP改善AD小鼠海马学习记忆能力及海马形态结构,通过抑制海马APP、Aβ1-42、IL-1β和TNF-α在AD治疗中发挥重要作用。

英文摘要：

Objective To explore the effect of Danxi Gout Party（ DGP） on hippocampal in Alzheimer ＇s disease（ AD）mice. Methods C57 BL /6 mice were randomly divided into control,model,treatment（ Piracetam 0. 42 g / kg）,DGP high-dose（ DGP52 g / kg）,DGP medial-dose（ DGP 26 g / kg）,DGP low-dose groups（ DGP 13 g / kg）. By using microinjection of 10 μg incubated amyloid beta1 - 42（ Aβ1 - 422 g / L） into the dorsal blade of the dentate gyrus in the bilateral hippocampus with intraperitoneal injection of D-galactose（ 180 mg/kg） in combination of mice to induce an AD mice. The mice were killed after 35 days continuous treating. After the treatment all animals were sacrificed. The Morris water maze was used to observe the learning and memory ability for the mice. Electron microscopy of hippocampus was observed. Biochemical methods were used to determine the content of β-amyloid protein precursor（ APP）,Aβ1 - 42,interleukin（ IL）-1β and tumor necrosis factor（ TNF）-α in the hippocampus tissue. Results Compared with the control group,latencies and swimming distances were significantly increased（ P〈0. 05）; target quadrant time and the number of cross-platform were significantly decreased（ P〈0. 05）; APP,Aβ1 - 42,IL-1β and TNF-α were significantly increased in model group（ P〈0. 05）. Compared with the model group,high-and medial-dose of DGP could significantly improve the learning,memory ability and morphological structure of hippocampus tissue of AD mice（ P〈0. 05）,APP,Aβ1 - 42,IL-1β and TNF-α in the hippocampus tissue were significantly decreased in high-and medial-dose of DGP groups（ P〈0. 05）. Conclusions DGP could improve the ability of learning,memory and morphological structure of the hippocampus tissue of AD mice. DGP plays a certain role in the treatment of AD through inhibiting APP,Aβ1 - 42,IL-1β and TNF-α.