Mouse DAI. (A) IP, intraperitoneal injection group; IV, intravenous injection group. After IP injection, the mice showed improvements in diarrhea and blood in the stool, but the effects in the IV group were not obvious. Mouse colon anatomy. (B): a1, IV group; a2, IP group; a3, model group; a4, normal control group. (C): b1, b2, b3 and b4 represent the mUCMSC group, hUCMSC group, model group and normal control group, respectively. Mouse survival curve. (D): M, IP, and IV represent the model group, hUCMSC IP group, and hUCMSC IV group, respectively. In the acute IBD study, the survival rates of M, IV, and IP were 83.3%, 91.7%, and 100%, respectively (n = 12). (E) In the chronic IBD study, the survival rates of the normal control group (n = 9), model group, mUCMSC group and hUCMSC group were 100%, 40%, 86.7%, and 100%, respectively (n = 15). Values represent the average of each group. Colon histopathological changes (HE staining) (100× magnification). (F) Normal control group; (G): Model group; (H): IV group; (I): IP group. In the IP and IV treatment groups, leukocyte infiltration was observed in the colon, but the intestinal wall edema was mild, and the degree of glandular damage was significantly lower than that in the model group. In the model group, the intestinal epithelial structure was disordered, and edema, epithelial necrosis, cellulose exudation, inflammatory cell infiltration, and intestinal lumen stenosis were observed. (J) Normal control group; (K): model group; (L): hUCMSC group; (M): mUCMSC group. Observations of colon tissue in the model group in the chronic IBD study revealed missing gland-like structures, an unclear layer of the intestinal wall, exuded cellulose, and the dense distribution of inflammatory cells in various layers of the intestinal wall. (K) The colon tissue of mice treated with UCMSCs was clearly visible, and the extent and density of inflammatory cell infiltration were inferior to those in the model group (L,M).