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Background Allergic rhinitis (AR) is a prevalent chronic inflammatory disorder characterized by persistent inflammation and nasal epithelial barrier disruption. Restoring epithelial integrity and modulating the inflammatory cascade are considered promising therapeutic strategies for AR. Purpose This study aims to systematically investigate the therapeutic efficacy of Yuping Tongqiao Tablet (YPTQ), a traditional Chinese medicine formula, in the treatment of AR and to decipher its potential mechanisms and active ingredients focusing on inflammation amelioration and barrier restoration. Methods An AR model was established in Sprague-Dawley rats that were sensitized and challenged with OVA. After intervention with different doses of YPTQ, nasal pathological injury and inflammatory cell infiltration were evaluated. In vitro , a human nasal epithelial cell (RPMI-2650) injury model was induced using house dust mites (HDM). Following YPTQ treatment, the expression levels of inflammatory factors and barrier-related proteins were assessed. Furthermore, the potential mechanisms and targets of YPTQ and its active monomers against AR were investigated by integrating network pharmacology analysis and molecular docking with in vitro experiments. Results In the OVA-induced AR rat model, YPTQ effectively alleviated nasal symptoms, reduced histopathological damage and inflammatory cell infiltration, and suppressed overall inflammatory levels. In the HDM-induced RPMI-2650 cell injury model, YPTQ significantly inhibited inflammatory cytokines release and upregulated the tight junction protein ZO-1, thereby enhancing epithelial barrier function. Moreover, integrated analysis combining network pharmacology, molecular docking, and both in vitro and in vivo validation confirmed that YPTQ and its active ingredient, kaempferol, exert therapeutic effects through two main pathways. Firstly, they down-regulated the expression of TSLP and inhibited the migration of DCs, which subsequently alleviated nasal inflammation. Secondly, they up-regulated and activated the expression of AhR and the downstream CYP1A1, which in turn promoted the expression of a barrier-associated protein, contributing to the restoration of nasal epithelial barrier integrity.
Wang et al. (Fri,) studied this question.