OBJECTIVE To observe the effects of curcumin on the gastric tissue morphology and inflammatory microenvironment in mice with gastric epithelia dysplasia (GED), and to evaluate the preventive and therapeutic effects of curcumin on GED. METHODS Normal control group, model group, low, medium, and high dose groups of curcumin, and positive control group were set up. Except for the normal control group, all other groups were induced to establish GED animal models using a compound factor modeling method. After 8 weeks of modeling, the low, medium, and high dose groups of curcumin and the positive control group were respectively given curcumin at doses of 38, 75, 150 mg·kg^-1 and vitacoenzyme 350 mg/kg for intervention, continued for 8 weeks. At the end of the experiment, the gastric levels of pepsinogen PGⅠ, IFN-γ, IL-1β, IL-6, and the relative expression levels of p-JAK2, p-STAT3, Cyclin D1 in each experimental group were detected. HE staining and PCNA antibody immunohistochemistry were performed to observe the gastric mucosal tissue morphology and cell proliferation in each group. The pathological scores of GED and inflammatory cell infiltration were evaluated, and the proliferation index (PI) was calculated. RESULTS Compared with the normal control group, the serum concentration of PGⅠ in mice in the model group decreased, while the levels of IL-1β, IFN-γ, and IL-6 in gastric tissue increased (P<0.05). The scores of GED and gastric mucosal inflammatory cell infiltration, as well as the proliferation index (PI), all increased (P<0.01). Histopathological observations revealed changes such as epithelial dysplasia and inflammatory cell infiltration in the gastric mucosa, enhanced cell proliferation activity, and upregulation of p-JAK2, p-STAT3, and Cyclin D1 expression (P<0.05). Compared with the model group, the medium and high dose groups of curcumin showed an increase in serum PG1 concentration, a decrease in the inflammatory factors IFN-γ and IL-6 levels in gastric tissue (P<0.05), a decrease in GED and gastric mucosal inflammatory cell infiltration scores, as well as PI (P<0.05 or 0.01). The curcumin treatment alleviated gastric mucosal dysplasia and inflammatory cell infiltration, inhibited cell proliferation activity, and downregulated the expression of p-JAK2, p-STAT3, and Cyclin D1 (P<0.05). In the low dose group of curcumin, the expression of p-JAK2 protein was downregulated, and in the high dose group, IL-1β decreased (P<0.05). CONCLUSION Curcumin has a preventive and alleviating effect on the epithelial dysplasia of the gastric mucosa in mice, and can improve the tissue morphology of the gastric mucosa in GED mice. Its mechanism of action may be related to the downregulation of the JAK2/STAT3/Cyclin D1 pathway signaling, inhibiting excessive cell proliferation.