目的:观察中药复方对慢性铝中毒老年痴呆小鼠学习记忆障碍的保护作用,探讨其对 M 受体含量的影响。方法:小鼠60只随机分为6组,空白组和模型组用蒸馏水灌胃,脑复康组用脑复康液420 mg/(kg·d)灌胃,中药大、中、小剂量组分别用中药复...目的:观察中药复方对慢性铝中毒老年痴呆小鼠学习记忆障碍的保护作用,探讨其对 M 受体含量的影响。方法:小鼠60只随机分为6组,空白组和模型组用蒸馏水灌胃,脑复康组用脑复康液420 mg/(kg·d)灌胃,中药大、中、小剂量组分别用中药复方浓缩煎液34 g/(kg·d),17 g/(kg·d),8.5 g/(kg·d)灌胃,共55天。除空白组外,所有动物复制慢性铝中毒老年痴呆模型,并在末次给药30 min 后以跳台法进行学习训练,记录潜伏期及错误次数。24 h 后再测记忆成绩,并检测皮层及海马 M 受体亚型含量。结果:模型组记忆潜伏期明显缩短(P<0.01),学习潜伏期明显延长(P<0.01),学习和记忆的错误次数明显增多(P<0.01);用药各组记忆潜伏期均明显延长(P<0.01),学习潜伏期明显缩短(P<0.05或P<0.01)。中药3个剂量组学习和记忆错误次数亦明显减少(P<0.05),脑复康组记忆错误次数无明显改善(P>0.05);用药各组除中药小剂量组外均有提高模型小鼠皮层与海马区 M_1受体亚型含量的作用(P<0.05或 P<0.01),但对M_2受体亚型含量无明显影响。结论:中药复方对氯化铝所致小鼠学习记忆障碍具有保护作用,能明显提高老年痴呆模型小鼠皮层及海马区 M_1受体含量。展开更多
Objective To identify the genetype of the PS1/APP double transgenie mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenie mice models and Aβ1-40-in...Objective To identify the genetype of the PS1/APP double transgenie mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenie mice models and Aβ1-40-injeeted rats models of Alzheimer disease. Methods The modified congo red staining, Nissl＇s staining and immunohistology staining was used to observe the Aβ deposits, activation of astrocyte respectively. Results ①The PS1/APP transgenic mouse extensively displayed Aβ deposits in the cortex and hippocampal structures, and GFAP positive cells were aggregated in mass and surrounded the congo red-positive plaque. ②The Aβ1-40-intrahippocmnpal-injeeted rat model showed the Aβ plaque deposits in the dentate gyrus of the hippocampus, with the astrocyte surrounded. The neurons loss was significant in the injection point and pin hole of injection with Nissl＇s staining methods. GFAP-positive cells increased significantly compared with the uninjected lateral of the hippocampus. Conclusion Although Aβ1-40-injected rat models could simulate some characteristic pathological features of human Alzheimer diseases, Aβ deposits and neurons loss in partial hippocampal, it would not simulate the progressive degenenration in the brain of AD. The double transgenie PS1/APP mice could simulate the specific pathogenesis and progressive changes of AD, mainly is Aβ deposits and the spongiocyte response , while no neurons loss were observed in this model.展开更多
文摘目的:观察中药复方对慢性铝中毒老年痴呆小鼠学习记忆障碍的保护作用,探讨其对 M 受体含量的影响。方法:小鼠60只随机分为6组,空白组和模型组用蒸馏水灌胃,脑复康组用脑复康液420 mg/(kg·d)灌胃,中药大、中、小剂量组分别用中药复方浓缩煎液34 g/(kg·d),17 g/(kg·d),8.5 g/(kg·d)灌胃,共55天。除空白组外,所有动物复制慢性铝中毒老年痴呆模型,并在末次给药30 min 后以跳台法进行学习训练,记录潜伏期及错误次数。24 h 后再测记忆成绩,并检测皮层及海马 M 受体亚型含量。结果:模型组记忆潜伏期明显缩短(P<0.01),学习潜伏期明显延长(P<0.01),学习和记忆的错误次数明显增多(P<0.01);用药各组记忆潜伏期均明显延长(P<0.01),学习潜伏期明显缩短(P<0.05或P<0.01)。中药3个剂量组学习和记忆错误次数亦明显减少(P<0.05),脑复康组记忆错误次数无明显改善(P>0.05);用药各组除中药小剂量组外均有提高模型小鼠皮层与海马区 M_1受体亚型含量的作用(P<0.05或 P<0.01),但对M_2受体亚型含量无明显影响。结论:中药复方对氯化铝所致小鼠学习记忆障碍具有保护作用,能明显提高老年痴呆模型小鼠皮层及海马区 M_1受体含量。
基金This project was supported by the National Natural Science Foundation of China （ No. 30100087, 30500148, 30571770）funded by the Collaborating Research Fund for Young Scholars from Abroad of National Natural Science Foundation of China （ No. 30228018 ）.
文摘Objective To identify the genetype of the PS1/APP double transgenie mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenie mice models and Aβ1-40-injeeted rats models of Alzheimer disease. Methods The modified congo red staining, Nissl＇s staining and immunohistology staining was used to observe the Aβ deposits, activation of astrocyte respectively. Results ①The PS1/APP transgenic mouse extensively displayed Aβ deposits in the cortex and hippocampal structures, and GFAP positive cells were aggregated in mass and surrounded the congo red-positive plaque. ②The Aβ1-40-intrahippocmnpal-injeeted rat model showed the Aβ plaque deposits in the dentate gyrus of the hippocampus, with the astrocyte surrounded. The neurons loss was significant in the injection point and pin hole of injection with Nissl＇s staining methods. GFAP-positive cells increased significantly compared with the uninjected lateral of the hippocampus. Conclusion Although Aβ1-40-injected rat models could simulate some characteristic pathological features of human Alzheimer diseases, Aβ deposits and neurons loss in partial hippocampal, it would not simulate the progressive degenenration in the brain of AD. The double transgenie PS1/APP mice could simulate the specific pathogenesis and progressive changes of AD, mainly is Aβ deposits and the spongiocyte response , while no neurons loss were observed in this model.
