Abstract: Objective To explore the therapeutic effect and mechanism of pachymic acid(PA) on Helicobacter pylori(Hp)-associated gastritis in rats. Methods A rat model of Hp-associated gastritis was established; all rats were separated into control group(CT group), model group(group M), PA low-dose group(PA L group), PA high-dose group(PA H group), and PA H+phosphatidylinositol 3-kinase(PI3K) activator(740 Y-P) group; the gastric mucosal injury index(UI) of rats in each group was evaluated, transmission electron microscopy was applied to observe the morphology of gastric mucosal cells. HE staining was applied to evaluate the pathological characteristics of gastric mucosa. ELISA was applied to detect the levels of interleukin-6(IL-6), tumor necrosis factor-α(TNF-α), IL-10, inducible nitric oxide synthase(iNOS), and superoxide dismutase(SOD) in gastric tissue. Western blot method was applied to detect the expression of PI3K, phosphorylated PI3K(p-PI3K), protein kinase B(AKT), p-AKT, nuclear factor(NF)-κB p65, and p-NF-κB p65 proteins. Results Compared with the CT group, the gastric mucosa erosion, epithelial edema, congestion, and severe ulcers were observed in the group M, with epithelial cell pyknosis and inflammatory cell infiltration, the UI, IL-6, TNF-α, iNOS, and the expression levels of p-PI3K/PI3K, p-AKT/AKT, p-NF-κB p65/NF-κB p65 proteins increased, the levels of IL-10 and SOD decreased(P＜0.05); compared with group M, the gastric mucosal damage and inflammatory cell infiltration in the PA L and PA H groups were improved, the UI, IL-6, TNF-α, iNOS by the host animal and the expression of p-PI3K/PI3K, p-AKT/AKT, p-NF-κB p65/NF-κB p65 proteins all decreased, the level of IL-10 and SOD was increased(P＜0.05); compared with the PA H group, the pathological damage of the gastric mucosa in the PA H+740 Y-P group was aggravated, with epithelial cell pyknosis. The UI, IL-6, TNF-α, iNOS, and the expression of p-PI3K/PI3K, p-AKT/AKT, p-NF-κB p65/NF-κB p65 proteins increased, the levels of IL-10 and SOD decreased(P＜0.05). Conclusions PA might facilitate the treatment of Hp-associated gastritis in rats by inhibiting the PI3K/AKT/NF-κB signaling pathway.

Key words: pachymic acid, Helicobacter pylori-associated gastritis, phosphatidylinositol 3-kinase/protein kinase B/nuclear factor-κB signaling pathway(PI3K/AKT/NF-κB)