Abstract
Abstract
Allergic rhinitis (AR) is a common chronic inflammatory disorder characterized by nasal mucosal inflammation, sneezing, and rhinorrhea. Schisandrin A (Schis-A) has demonstrated significant anti-inflammatory effects in models of allergic asthma. This study aimed to evaluate the therapeutic efficacy of Schis-A in AR and to elucidate its underlying molecular mechanisms. An AR mouse model was established by sensitization and challenge with ovalbumin (OVA), followed by oral administration of Schis-A at doses of 40 and 80 mg/kg/day. Nasal symptoms were monitored and quantified. OVA-specific immunoglobulin E (IgE) levels and T helper (Th)1/Th2- and regulatory T cells (Treg)/Th17-associated cytokines were measured using enzyme-linked immunosorbent assay and quantitative real-time PCR. Treg and Th17 cell populations were analyzed by flow cytometry. The results showed that Schis-A treatment significantly reduced OVA-induced nasal rubbing and sneezing, indicating effective attenuation of allergic responses. Serum OVA-specific IgE levels were markedly reduced in Schis-A-treated AR mice. Moreover, Schis-A restored Th1/Th2 and Treg/Th17 cytokine balance, as indicated by upregulated expression of IFN-γ, IL-2, and Foxp3, alongside downregulation of IL-4, IL-5, IL-13, and IL-17. Flow cytometric analysis confirmed an increase in Treg cells and a reduction in Th17 cell populations. Mechanistically, Schis-A inhibited activation of the PI3K/AKT signaling pathway, suggesting that this pathway may contribute to its immunomodulatory effects. Schis-A alleviates AR by modulating Th1/Th2 and Treg/Th17 immune responses and inhibiting PI3K/AKT pathway activation, offering a promising therapeutic strategy for the treatment of AR.