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논문 기본 정보

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학술저널
저자정보
Liu Peiqiang (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Qin Danxue (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Lv Hao (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Fan Wenjun (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Zhou Fangwei (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Gao Ziang (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Tao Zezhang (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.) Xu Yu (Department of Otolaryngology-Head and Neck Surgery Renmin Hospital of Wuhan University Wuhan China.)
저널정보
대한천식알레르기학회(구 대한알레르기학회) Allergy, Asthma & Immunology Research Allergy, Asthma & Immunology Research Vol.13 No.6
발행연도
2021.11
수록면
882 - 895 (14page)
DOI
10.4168/aair.2021.13.6.882

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Purpose: Allergic rhinitis (AR) is a common otolaryngology disease and one of the clinical causes of olfactory dysfunction (OD). The olfactory bulb serves as a transfer station for olfactory information transmission, and alleviating its neuroinflammation may be expected to improve AR-induced OD. Recent studies have suggested that the dopamine D2 receptor acts as a key target in regulating immune functions and neuroinflammatory reaction. However, the effect of dopamine D2 receptor on AR-induced neuroinflammation is still unknown. Methods: An AR mouse model with OD induced by ovalbumin were constructed. The buried food pellet test was to evaluate the olfactory function of the mice. Immunofluorescence staining, hematoxylin and eosin staining, enzyme-linked immunosorbent assay and western blotting were also used to investigate the molecular mechanisms underlying the antiinflammatory effects of the dopamine D2 receptor in AR-induced OD. Results: We found that AR-induced OD has a relationship with inflammatory responses in the olfactory bulb. Nasal administration of quinpirole (Quin, a dopamine D2 receptor agonist, 3 mg/kg) improved olfactory function in mice, inhibited the expression of toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signalings and the levels of tumor necrosis factor-α, interleukin (IL)-1β and IL-6 in the olfactory bulb. In vitro, Quin (20 μmol/L) inhibited the release of TLR4/NF-κB signalings-dependent inflammatory cytokines in cultured microglia. Conclusions: Activation of the dopamine D2 receptor inhibits the release of inflammatory cytokines through TLR4/NF-κB signaling in the olfactory bulb microglia, and protects olfactory function.

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