Involvement of the miR-210-3P/Gbp3 Axis in NLRP3 Inflammasome modulation by Royal Jelly Acid in ulcerative colitis therapy

Royal jelly acid (RJA), the primary active component of royal jelly, exhibits notable immunomodulatory and anti-inflammatory properties. This study investigated the effects of RJA, administered via oral gavage, on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. In a DSS-induced murine UC model, RJA treatment improved colitis severity. High-throughput sequencing revealed alterations in miRNA and mRNA expression profiles, building an miRNA-mRNA interaction network to identify the key roles of miR-210-3P/Gbp3. Validation confirmed that RJA modulated the NLRP3-mediated pyroptosis pathway through the miR-210-3P/Gbp3 axis, significantly inhibiting the expression and translation of multiple inflammatory factors (IL-6, IL-1 β , IL-18, TNF- α ) ( p < 0.05). In vitro, RJA significantly reduced the expression of NLRP3 inflammasome-related proteins (NLRP3, Caspase-1, GSDMD, GSDMD-N) ( p < 0.05) and inhibited LPS-induced pyroptosis in RAW264.7 cells. These findings suggested that RJA exerts therapeutic effects on UC by targeting the miR-210-3P/Gbp3 axis and regulating the NLRP3 inflammasome. • RJA alleviates DSS-induced UC by modulating miR-210-3P/Gbp3 axis. • RJA inhibits NLRP3 inflammasome-mediated pyroptosis, reducing inflammation. • miR-210-3P directly targets Gbp3 to regulate inflammasome activity. • RJA shows potential as a therapeutic agent for Ulcerative Colitis.