Abstract
ObjectiveThis study aimed to investigate the effect of the p38 mitogen‐activated protein kinase (p38MAPK) signaling pathway on olfactory mucosa function and apoptosis of olfactory sensory neurons (OSNs) in an allergic rhinitis (AR) mouse model.MethodFifty‐five BALB/c mice were used to establish AR models by ovalbumin, and their olfactory function was confirmed by the buried food pellet test. Then, 28 mice with hyposmia were selected. SB203580, a p38MAPK inhibitor, and normal saline (NS) were injected into mice with olfactory defects. The olfactory function, apoptosis of OSNs in olfactory mucosa, and the expression of the olfaction marker protein (OMP), p38MAPK, and p‐p38MAPK were detected after the intervention.ResultSB203580 treatment significantly upregulated OMP expression and significantly improved the olfactory function of AR mice by reducing the percentage of apoptotic OSNs. In addition, SB203580 attenuated the activation of the p38MAPK signaling pathway.ConclusionSB203580 protected olfactory function in an AR mouse model. This protective effect may be associated with the antiapoptotic effects of SB203580 via the p38MAPK signaling pathway.
Highlights
Allergic rhinitis (AR) is an allergic disease with increasing morbidity, and olfactory dysfunction is a key symptom of patients with allergic rhinitis (AR)
The levels of ovalbu‐ min (OVA)‐sIgE and IL‐4 in the AR models significantly increased compared with those of the control group, which indicated that the AR mouse model was successfully established
We examined the expression of olfaction marker protein (OMP), brown nuclear staining, and the number and layers of OMP on olfactory epithelium (OE) after SB203580 treat‐ ment and found that these factors were significantly increased, and the staining was darker than that of the dysosmia epithelium in the normal saline (NS) and dimethyl sulfoxide (DMSO) groups (Figure 4a,b)
Summary
Allergic rhinitis (AR) is an allergic disease with increasing morbidity, and olfactory dysfunction is a key symptom of patients with AR. In both seasonal and perennial AR, different proportions and degrees of olfactory dysfunction have been reported. Olfactory function is a key contributor to quality of life (Croy, Nordin, & Hummel, 2014; Stevenson, 2010). When other symptoms of AR recov‐ ered after treatment, there were still some patients whose olfactory dysfunction could not be improved and remained, which has become the most difficult complication of AR to address
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