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

作者：Mingchuan Wang, Mengyuan Wang, Xinyi Gao, Huijie Xiao, Xianbin Cheng, Yunsheng Bai, Junwei Shao, Jialin Wang, Yang Jiang · 发表于：Journal of Functional Foods · 年份：2025 · DOI：10.1016/j.jff.2025.106791 · 被引用次数：2 · 研究领域：Inflammasome and immune disorders、Nigella sativa pharmacological applications、Tryptophan and brain disorders

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.