Erianin regulates allergic rhinitis via KAT2A-mediated histone succinylation.

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.