The objective of this study was to examine the impact and underlying mechanisms of pelargonidin-3-galactoside (Pg3gal) produced from purple sweet potatoes on colonic inflammation induced by dextran sulfate sodium (DSS)in a murine model of ulcerative colitis (UC). C57BL/6J mice were categorized into four groups (n = 6 per group):DSS+Pg3gal, control, control+Pg3gal, and DSS. Colitis was induced by providing free access to 3% DSS for 10 days. TheDSS+Pg3gal model mice received DSS concurrently with intragastric Pg3gal (25 mg/kg). The health of the mice was carefullymonitored on a regular basis, and scores for the Disease Activity Index (DAI) were documented. A histological assessmentwas conducted using hematoxylin and eosin staining to evaluate the extent of mucosal injury present. The expression levels ofIL-6, NLRP3, ASC, cleaved-Caspase-1, TNF-a, N-GSDMS, and cleaved-IL-1b proteins were evaluated by Western blotanalysis. The process of 16S rRNA sequencing was carried out to examine the composition and relative abundance of gutmicrobiotas within the intestines of the mice. The DAI results revealed that Pg3gal significantly attenuated the DSS-inducedUC in mice. In addition, it successfully alleviated the decline in colon size, improved the condition of colonic tissue, andsignificantly inhibited the production of proinflammatory cytokines, such as IL-6, IL-1b, and TNF-a, in the colon tissues. Additionally, Pg3gal modulated the DSS-induced imbalanced gut microbiota, as evidenced by decreased Proteobacteria andDeferribacteres and simultaneous elevation in Firmicutes, Bacteroidetes, and Verrucomicrobia. In summary, Pg3gal alleviatedDSS-induced UC by inhibiting pyroptosis in intestinal epithelial cells and enhancing the structural integrity of the gutmicrobiota.