Chien-Fu Yeh1,2,3, Tung-Yueh Chuang4, Ming-Ying Lan1,2, Yu-Ching Chin5, Wei-Hsin Wang6, Yung-Yang Lin7,4,8,9,10. 1. Department of Otolaryngology-Head and Neck Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C. 2. Department of Otorhinolaryngology, National Yang-Ming University, Taipei, Taiwan, R.O.C. 3. Institute of Brain Science, National Yang-Ming University, Taipei, Taiwan, R.O.C. 4. Department of Critical Care Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C. 5. Department of Medical Education, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C. 6. Department of Neurosurgery, Taipei Veterans General Hospital, School of Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C. 7. Institute of Brain Science, National Yang-Ming University, Taipei, Taiwan, R.O.C. yylin@vghtpe.gov.tw. 8. Institute of Physiology, National Yang-Ming University, Taipei, Taiwan, R.O.C. 9. Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C. 10. Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C.
Abstract
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. Copyright
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. Copyright
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