Key Results
In mice with DSS-induced ulcerative colitis, TBⅡ treatment repaired the intestinal mucosal barrier and alleviated colonic inflammation. RNA-seq analysis and levels of protein expression demonstrated that TBⅡ could prominently inhibit NLRP3 signaling. TBⅡ-mediated NLRP3 inhibition was associated with the alleviation of intestinal permeability and the inflammatory response via blocking the communication between epithelial cells and macrophages. However, pharmacological inhibition of NLRP3 or NLRP3 overexpression significantly impaired TBⅡ-mediated the anti-inflammatory effect. Mechanistically, TBⅡ-mediated NLRP3 inhibition may be partially associated with the suppression of NF-κB.