Knockdown ofalleviates ovalbumin-induced allergic rhinitis in mice by regulating NF-κB pathway.

Abstract

Allergic rhinitis (AR), a type of chronic inflammatory disease that exists in the nasal mucosa, significantly impacts the quality of life.gene encodes an RNA helicase belonging to the DEAD-box protein family and is part of the DDX3 subfamily that affects the progression of multiple diseases. However, the specific role and mechanisms ofin AR remain unclear. This study investigates the effects ofknockdown on ovalbumin (OVA)-induced AR in mice. We found thatis highly expressed in the nasal mucosa of AR mice. Knockdown ofin OVA-induced AR mice significantly alleviated nasal manifestations, reduced immunoglobulin E and histamine levels, and improved nasal mucosal histopathology. Additionally, knockdown ofsuppressed secretion of inflammatory factor nuclear factor kappa B (NF-κB) phosphorylation, thereby mitigating local inflammatory responses. These findings suggested that targetingcould offer a novel therapeutic strategy for managing AR by modulating the NF-κB pathway.