[Effect of schaftoside in inhibiting aspirin-induced gastric mucosal injury by targeting PYGB].

This study investigated the effect and mechanism of schaftoside(Xftg) against aspirin-induced gastric mucosal injury in mice. Aspirin-induced human gastric mucosal epithelial cell(GES-1) model and gastric mucosal injury model of mice were employed. The CCK-8 assay was used to detect the impact of different concentrations of Xftg on the viability of GES-1. Cell morphology was detected by using Hoechst 33342 fluorescent staining. Hematoxylin-eosin(HE) staining was employed to observe the mouse gastric tissue morphology. The expression levels of zonula occludens-1(ZO-1) and Occludin were detected by immunofluorescence. Mucin 2(MUC2) expression was measured via immunohistochemistry. Levels of interleukin(IL)-6, IL-1β, tumor necrosis factor-α(TNF-α), cyclooxygenase(COX)-1, and prostaglandin E2(PGE2) in serum were determined by enzyme-linked immunosorbent assay(ELISA). Target proteins were screened by using limited enzymatic digestion. The level of glycogen phosphorylase B(PYGB) in gastric tissue was determined by ELISA. Protein expression in gastric tissues was detected by Western blot. The results show that Xftg in vitro increases the viability and ameliorates nuclear fragmentation of aspirin-induced GES-1. In vivo, Xftg alleviates the weight loss of model mice with gastric mucosa injury and pathological damage of the gastric mucosa. It also increases the expression of Occludin and ZO-1 proteins in gastric tissue, normalizes MUC2 protein expression, elevates levels of COX-1 and PGE2 in serum, and reduces levels of IL-6, IL-1β, and TNF-α in serum. PYGB is identified as a potential target of Xftg by using limited enzymatic digestion. ELISA and Western blot experiments confirm that Xftg significantly downregulates PYGB protein expression in the gastric tissue of mice. In conclusion, Xftg may inhibit aspirin-induced gastric mucosal injury effect by targeting PYGB and downregulating PYGB protein expression.