Objective  To explore the impact of allergic rhinitis (AR) on olfactory function and observe the effectiveness of betamethasone in treating mice with olfactory dysfunction.

  Methods  Mouse AR models were established by intraperitoneal injection and intranasal application of ovalubumin. The olfactory function of the mice was evaluated by buried food test (BFT). The expression of olfactory marker protein (OMP) in the olfactory mucosa was tested by immunohistochamistry. The expression of OMP in the olfactory mucosa was observed 7 and 14 days after intraperitoneal application of betamethasone.

  Results  The incidence of olfactory dysfunction in AR mice was 74.55%. The olfactory epithelium became thinner in AR mice than in control group. The down-regulation of OMP in olfactory epithelium was observed in AR mice compared with control group. The number of OMP-positive cells was 66.38±1.517 in control group and 59.50±0.558 in group without olfactory dysfunction (P > 0.05). The number of OMP-positive cells was 39.77±2.012 in group with olfactory dysfunction, which was significantly different compared with control group and the group with olfactory dysfunction (P < 0.05). The number of OMP-positive cells was 62.04±1.227 in betamethasone group 1, which was significantly higher than that in the non-medication group (47.34±1.809) (P < 0.05); meanwhile, it showed no significant difference between betamethasone group 1 and the control group (P > 0.05). The number of OMP-positive cells was 63.82±1.254 in betamethasone group 2, and the expression of OMP in betamethasone group 2 was similar to that in betamethasone group 1.

  Conclusions  AR-associated olfactory dysfunction is not only due to the blockage of nasal cavity but also the change in mucosa by inflammation. Systemic application of betamethasone is an effective method in treating AR-associated olfactory dysfunction.