中风后嗅球过度表达小胶质细胞/巨噬细胞和促炎介质及嗅觉功能障碍。
Excessive Expression of Microglia/Macrophage and Proinflammatory Mediators in Olfactory Bulb and Olfactory Dysfunction After Stroke.
机构信息
Department of Otolaryngology-Head and Neck Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C.
Department of Otorhinolaryngology, National Yang-Ming University, Taipei, Taiwan, R.O.C.
出版信息
In Vivo. 2019 Nov-Dec;33(6):1893-1899. doi: 10.21873/invivo.11683.
BACKGROUND/AIM: Olfactory dysfunction can be caused by stroke but the pathogenesis is still unclear. Previous studies have proved that olfactory dysfunction could be caused by microglia activation in the olfactory bulb and that middle cerebral artery occlusion (MCAO) may induce ipsilateral olfactory bulb microglia activation. This study aimed to explore the possible pathogenesis of ischemic stroke-induced olfactory dysfunction.
MATERIALS AND METHODS
We used a rat model of MCAO to simulate ischemic stroke. Olfactory function tests were performed using buried food test. The mRNA expression of olfactory marker protein (OMP), microglia/macrophage activation, and proinflammatory mediators were measured using reverse transcription-quantitative polymerase chain reaction.
RESULTS
Following MCAO, rats had poorer olfactory performance. In the olfactory bulb of the rats, the mRNA expression of OMP decreased and the mRNA expression of microglia/macrophage activation and proinflammatory mediators increased.
CONCLUSION
Ischemic stroke causes microglia/macrophage activation and promotes neuroinflammation in the olfactory bulb, causing olfactory dysfunction.
背景/目的：嗅觉功能障碍可由中风引起，但发病机制尚不清楚。先前的研究已经证明，嗅觉功能障碍可能是嗅球中小胶质细胞的激活引起的，而大脑中动脉阻塞（MCAO）可能会导致同侧嗅球小胶质细胞的激活。本研究旨在探讨缺血性中风引起的嗅觉功能障碍的可能发病机制。
材料和方法
我们使用 MCAO 大鼠模型模拟缺血性中风。使用埋藏食物试验进行嗅觉功能测试。使用逆转录定量聚合酶链反应测量嗅觉标记蛋白（OMP）的 mRNA 表达、小胶质细胞/巨噬细胞的激活和促炎介质。
结果
MCAO 后，大鼠的嗅觉表现变差。在大鼠嗅球中，OMP 的 mRNA 表达下降，小胶质细胞/巨噬细胞激活和促炎介质的 mRNA 表达增加。
结论
缺血性中风导致小胶质细胞/巨噬细胞激活，并促进嗅球中的神经炎症，导致嗅觉功能障碍。
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