In this study, we demonstrated the molecular mechanism of calycosin-regulated NLRP3-IL-33/ST2 signaling in intestinal fibrosis in IBD from the perspective of abnormal inflammatory immune regulation, and explored the value of calycosin in combination with targeted inhibitors of NLRP3 signaling in the treatment of IBD. The gene discussed is NLRP3; the disease is inflammatory bowel disease.