The protective effects and mechanisms of Erucic acid in allergic rhinitis via the MyD88/NF-κB pathway.

Allergic rhinitis (AR), a local inflammatory disease mediated by IgE in the nasal mucosa, presents a significant challenge to global health. Erucic acid (EA) is a monounsaturated fatty acid. Current research indicates EA possesses diverse biological activities, including anti-inflammatory, antioxidant, and immunomodulatory properties. However, its effects on AR remain unexplored. This study aims to investigate the therapeutic action and mechanism of EA in AR. The efficacy and mechanisms of EA were evaluated on the AR mouse model. Therapeutic outcomes were assessed through behavioral observations, measurements of various related cytokines in nasal mucosa and serum, and histopathological examination of nasal mucosa. An in vitro inflammatory model was established in RAW264.7 cells to investigate the anti-inflammatory effects and mechanisms of EA via RT-qPCR and Western blot. This study shows that, at a safe dose, EA significantly alleviates AR-associated behaviors such as rubbing and sneezing and reduces serum levels of histamine, Ovalbumin-specific IgE (OVA-sIgE), inflammatory cytokines, and chemokines. EA mitigated damage to the nasal mucosa tissue, including an increase of goblet cells, mast cells, and eosinophils. In the nasal tissue, EA also downregulated the mRNA levels of inflammation-related factors and epithelial barrier-related factors, as well as the protein levels of Myeloid Differentiation Primary Response Protein 88 (MyD88) and NF-κB. In vitro, EA suppressed Lipopolysaccharide (LPS)-induced expression of inflammatory cytokines and inhibited activation of the MyD88/NF-κB pathway. These findings demonstrate that EA exerts anti-inflammatory and epithelial barrier-restorative effects through inhibiting the MyD88/NF-κB pathway.