设为首页
加入收藏
联系我们
Email-Alert
 

    首页 | 杂志介绍 | 编委成员 | 审稿专家名录 | 投稿指南 | 订阅指南 | 过刊浏览 | 论著模板 | 综述模板 | 帮助

 
李明月,陶玉倩,胡昔权,张丽颖,吴腾腾,裴 中.阿尔兹海默病小鼠不同时期脑血管的功能改变及机制[J].中国康复医学杂志,2019,(10):1143~1149
阿尔兹海默病小鼠不同时期脑血管的功能改变及机制    点此下载全文
李明月  陶玉倩  胡昔权  张丽颖  吴腾腾  裴 中
中山大学附属第三医院康复医学科,广东省广州市,510630
基金项目:广东省自然科学基金项目(2016A030313193); 国家自然科学基金青年基金项目(81601979)
DOI:
摘要点击次数: 200
全文下载次数: 123
摘要:
      摘要 目的:研究散发性阿尔兹海默病(sAD)小鼠模型早期、中期脑血管功能改变及机制。 方法:通过脑室内注射链脲霉素建立sAD模型,造模2周后采用Morris水迷宫评估小鼠认知功能,验证模型成立;利用活体成像技术检测假手术组、早期组(造模1周)、中期组(造模3个月)小鼠脑皮层动脉、穿支动脉、静脉及毛细血管对短暂高碳酸血症的血管反应性,并分别使用一氧化氮合酶抑制剂L-NAME及前列腺素合成抑制剂吲哚美辛阻断其相关通路,观察各组同种血管反应性变化。 结果:与假手术组相比,造模2周后sAD小鼠学习、空间记忆能力显著下降。与假手术组相比,造模1周小鼠的脑皮层动脉、毛细血管的反应性均显著下降,皮层动脉反应性于造模3个月时恢复,而毛细血管反应性无明显恢复。L-NAME可显著增加sAD小鼠脑动脉、毛细血管反应性。吲哚美辛可明显减弱sAD小鼠脑动脉反应性,但对毛细血管无影响。 结论:sAD小鼠早期存在的脑血管功能损伤,可能参与认知障碍的发生和发展,其机制与一氧化氮通路改变有关。
关键词:散发性阿尔兹海默病  认知障碍  脑血管反应性  一氧化氮
A study on cerebrovascular dysfunction in mouse model of Alzheimer's disease during different stage    Download Fulltext
Department of Rehabilitation, The Third Affiliated Hospital of Sun Yat-Sen University, Guangdong, Guangzhou, 510630
Fund Project:
Abstract:
      Abstract Objective:To study the functional changes of cerebrovascular in sporadic Alzheimer's disease(sAD) mice in the early and middle stage and to explore the related mechanism. Method:sAD mice were induced by intraventricular injection of streptozotocin, and the cognitive function of the mice was evaluated by Morris water maze 2 weeks after operation. Two-photon in vivo imaging was used to measure the dilatation response of surface arteries, penetrating arteries, veins and capillaries responsing to 5% CO2 inhalation for 1 minute under thinned-cranial window in control group, sham operation group, early (1 week) and middle group (3 months). L-NAME,an inhibitor of nitric oxide (NO) synthase, Indomethacin, and an inhibitor of prostaglandin (PG) synthesis, were used to block the vasodilation pathway. The vasodilation reaction was repeatedly observed and compared between each group. Result:Two weeks later, the sAD mice model showed learning and spatial memory impairment compared with sham operation group. One week after modeling, the cerebral capillary responsiveness decreased and persisted, the cerebral artery responsiveness of mice model group decreased than that of sham operation group, and recovered after 3 months. Compared between the sham operation group and the model group, indomethacin could reduce the cerebral arterial reactivity to the same extent, but not affect the capillary reactivity of each group. L-NAME could weaken all types of cerebrovascular reactivity of the sham operation group, but not affect the model group. Conclusion:The early onset of cerebrovascular dysfunction in sAD mice may be involved in the occurrence and development of cognitive impairment in mice; the damage mechanism is related to the changes of NO pathway dysfunction.
Keywords:sporadic Alzheimer's disease  cognitive impairment  cerebrovascular reactivity  NO
查看全文  查看/发表评论  下载PDF阅读器

您是本站第 23131052 位访问者

版权所有:中国康复医学会
主管单位:国家卫生健康委员会 主办单位:中国康复医学会
地址:北京市朝阳区樱花园东街,中日友好医院内   邮政编码:100029   电话:010-64218095   

本系统由北京勤云科技发展有限公司设计 京ICP备18060696号-2