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.