| 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： |
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| 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 |
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| Department of Rehabilitation, The Third Affiliated Hospital of Sun Yat-Sen University, Guangdong, Guangzhou, 510630 |
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| 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 |
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