Objective To investigate the effect of naringenin on the expression of miR-30a-3p/PTEN signal axis in the intestinal tissue of mice with ulcerative colitis. Methods Ulcerative colitis model of BALB/c mice was prepared by DSS gavage method. The negative control group and model group were gavaged with normal saline(0.2 mL/10g), and the positive control group was gavaged with prednisolone(2 mg/kg). The low, middle and high-dose naringenin groups were given naringenin by intragastric administration(the doses were 50, 100, and 200mg/kg) for 7 days. The disease activity score(DAI) was calculated, morphological examination of intestinal tissue in BALB/c mice performed evaluated, and Elisa was used to detect the levels of IL-4, IL-10, and TNF-α in intestinal tissue, RT-PCR and Elisa method measure the levels of miR-30a-3p, PTEN, PI3K, Akt and Caspase-3 mRNA and protein in intestinal tissue respectively. Results The mouse colon in the model group had partial intestinal wall depression, formation of ulcers, obvious edema in the surrounding tissues, necrosis and shedding of some cells, and inflammatory cell infiltration. The damage of colon tissue pathology of the mice in the positive control group and each naringenin dosage group was significantly improved compared with the model group. Compared with the negative control group, DAI, IL-4, TNF-α, PTEN and Caspase-3 mRNA and protein in the intestinal tissues of the other groups of mice increased, and IL-10, miR-30a-3p, PI3K and Akt mRNA and protein decreased(P＜0.05). Compared with the model group, the DAI, IL-4, TNF-α, PTEN and Caspase-3 mRNA and protein of mice in the positive control group and each naringenin dose group decreased, IL-10, miR-30a-3p, PI3K and Akt mRNA and protein increased, and the effects of each naringenin dose group showed a dose-response relationship(P＜0.05). There was no significant difference in indicators between the high-dose naringenin group and the positive control group(P＞0.05). Conclusion Naringenin can reduce colitis and pathological damage in mice with ulcerative colitis. The mechanism may be related to the regulation of miR-30a-3p/PTEN signal axis.