Excessive Expression of Microglia/Macrophage and Proinflammatory Mediators in Olfactory Bulb and Olfactory Dysfunction After Stroke

In Vivo. 2019 Nov-Dec;33(6):1893-1899. doi: 10.21873/invivo.11683.

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.

Keywords: Olfactory dysfunction; ischemic stroke; macrophage; microglia; middle cerebral artery occlusion; proinflammatory mediator; rat.

MeSH terms

  • Animals
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Female
  • Infarction, Middle Cerebral Artery / metabolism
  • Inflammation / metabolism*
  • Macrophages / metabolism*
  • Male
  • Microglia / metabolism*
  • Olfactory Bulb / metabolism*
  • Olfactory Marker Protein / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred WKY
  • Stroke / metabolism*

Substances

  • Cytokines
  • Olfactory Marker Protein
  • RNA, Messenger