Intranasal application of glucocorticoid alleviates olfactory dysfunction in mice with allergic rhinitis.

The aim of the present study was to investigate the effect of glucocorticoid intervention on olfactory dysfunction in mice with allergic rhinitis (AR). An AR animal model was established by intraperitoneal injection and intranasal application of ovalbumin to mice. The olfactory function of the mice was evaluated using a buried food test, and morphological changes in the nasal mucosa were determined using hematoxylin and eosin staining. The expression of olfactory marker protein (OMP) in the olfactory mucosa was tested by immunohistochemistry, and was observed on days 7 and 14 after the application of glucocorticoid. The incidence rate of olfactory dysfunction in AR mice was 75.34%, and the olfactory epithelium became thinner in mice with AR compared to the control group. In addition, the expression of OMP in the olfactory epithelium was downregulated in mice with AR compared with the control group. Expression of OMP in the olfactory epithelium was upregulated in the budesonide group A and betamethasone group A compared with the medicine-free group, whereas the expression of OMP in the olfactory epithelium of budesonide group A or betamethasone group A was not significantly different from the control group. Moreover, the expression of OMP in the budesonide group B was similar to budesonide group A, and expression of OMP in betamethasone group B was similar to betamethasone group A. The expression of OMP in olfactory mucosa is downregulated in AR mice with olfactory dysfunction. Following the application of glucocorticoid, the expression of OMP in the olfactory mucosa in mice is upregulated. Moreover, intranasal local glucocorticoid has a low incidence of systemic adverse reactions, and is recommended for the treatment of olfactory dysfunction in AR.