Abstract
BACKGROUND: Allergic rhinitis arthritis (AR) is a common chronic inflammatory disease, which may lead to other systemic chronic diseases. Erianin, a natural product isolated from Dendrobium chrysotoxum, has been reported to exert effects on a variety of diseases. In this work, we aimed to explore the effects and mechanisms of erianin in allergic rhinitis. METHODS: Interleukin-13 (IL-13) was selected to treat nasal epithelial cells (NECs) to establish an in vitro AR model; Ovalbumin (OVA) was used to treat the nasal cavity of mice to establish an in vivo AR model; Cell counting kit 8 (CCK-8) was used to detect the cell activity of nasal epithelial cells after different treatments; Apoptosis and inflammatory cell infiltration of nasal tissue were analyzed by TUNEL and H&E staining, respectively; Mice noses scratching were counted to determine the severity of inflammation; Inflammation-related cytokine expression was examined by qPCR and ELISA to determine how erianin alleviates inflammation; Changes in apoptosis and histone acetylation succinylation modification were examined by Western blotting; Enrichment of KAT2A and histone succinylation at the p65 promoter was detected by ChIP-seq. RESULTS: Erianin inhibited IL-13-induced inflammation in nasal epithelial cells in vitro, while alleviating OVA-induced rhinitis in mice in vivo. In further mechanistic studies, Erianin was found to regulate the disease through KAT2A-mediated histone succinylation. Erianin blocked KAT2A as well as H3K79 succinylation and further inhibited p65 expression, thereby controlling the further development of allergic rhinitis. CONCLUSION: Erianin alleviates and inhibits allergic rhinitis through KAT2A-mediated histone succinylation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12950-025-00479-1.