Calycosin prevents NLRP3-induced gut fibrosis by regulating IL-33/ST2 axis

• DOI: 10.1016/j.heliyon.2024.e30240
• Publication Date: 2024-04-25T03:38:24Z
• Authors: Xiujun Liao; Haiting Xie; Saojun Yu
• Keywords: Calycosin

Intestinal interstitial fibrosis is a core event of inflammatory bowel disease (IBD) development. Calycosin has been recognized to carry various therapeutic bioactivities. However, the role calycosin in intestinal remains be illustrated. This aim this study was explore effects on IBD and underlying mechanisms. The vitro vivo models were established by using TNBS-induced mouse model co-culture epithelial cells cells; moreover, lentivirus-mediated knockdown NLRP3 expression applied. results showed that significantly improved IBD. Mechanistically, downregulated inhibited activation IL-33/ST2 signaling cells, which subsequently impedes cell migration regulating secretion signaling-induced mediators. Notably, combination blockade extent. Altogether, suggests can improve downregulating NLRP3-IL-33/ST2 signaling, reducing inflammation decreasing pro-fibrotic factors' secretion, provides new perspective for options