Objective To explore the factors associated with the pathogenesis of gastric ulcer and mechanism of inflammatory response in a mouse model.

Methods A total of 31 patients with gastric ulcer were enrolled in the ulcer group, and 31 healthy individuals undergoing physical examinations during the same period were included in healthy group. The infection status of Helicobacter pylori (Hp), serum levels of inflammatory cytokines and T-lymphocyte subset indicators were compared between the two groups. Logistic regression analysis was employed to screen for the influencing factors of gastric ulcer onset. A lipopolysaccharide (LPS) -induced gastric injury mouse model was constructed, and the levels of relevant inflammatory cytokines after chlorogenic acid intervention were measured.

Results The Hp infection level in the healthy group was lower than that in the ulcer group, and the difference was statistically significant (t=5.95, P < 0.001). The levels of interleukin (IL)-2, IL-5, IL-8, IL-12p70, IL-17A, interferon-α (IFN-α) and tumor necrosis factor-α (TNF-α) in the ulcer group were higher than those in the healthy group, with statistically significant differences (P < 0.05). The counts of cluster of differentiation 45-positive lymphocytes (CD45⁺Lym), T-lymphocytes (CD3⁺), helper/inducer T-lymphocytes (CD3⁺CD4⁺), suppressor/cytotoxic T-lymphocytes (CD3⁺CD8⁺) and the percentages of helper/inducer T-lymphocytes (CD3⁺CD4⁺%) in the ulcer group were lower than those in the healthy group, and the differences were statistically significant (P < 0.05). Logistic multivariate regression analysis revealed that Hp infection, elevated IL-12p70 and elevated TNF-α were independent risk factors for the onset of gastric ulcer (P < 0.05). In the LPS-induced gastric injury mouse model, chlorogenic acid intervention significantly inhibited increase in the expression levels of IL-6, IL-1β, IL-12 and TNF-α in mouse plasma (P < 0.05).

Conclusion Patients with gastric ulcer exhibit high expression of Hp, IL-12p70 and TNF-α, which are important influencing factors for the pathogenesis of gastric ulcer. In addition, chlorogenic acid can effectively inhibit the elevation of inflammatory cytokine levels in mice with LPS-induced gastric injury.