Gastroprotective effects of a traditional ginseng–ginger formulation in a stress-induced gastritis mouse model

This study investigated the gastroprotective effects of a formulation combining extracts of Panax ginseng C.A.Mey. and Zingiber officinale Roscoe (PZ) in a mouse model of water immersion and restraint stress (WIRS)-induced gastritis. In an exploratory ratio-screening experiment, the 3:1 ginseng-to-ginger formulation significantly reduced gastric hemorrhagic lesions relative to the WIRS group and was therefore selected as a representative active formulation for subsequent dose-ranging and mechanistic studies. Because this screening was exploratory, the 3:1 formulation was selected based on its activity relative to the WIRS group rather than on a formal comparison of superiority among the formulations. Seven-day oral administration of the selected formulation significantly reduced gastric interleukin-1β, inducible nitric oxide synthase, and cyclooxygenase-2 protein abundance relative to the DW-treated WIRS group. The formulation also reduced lipid peroxidation and increased glutathione peroxidase activity, consistent with enhanced antioxidant defense. The formulation did not significantly affect the mRNA expression of M3R, H2R, or CCK2R. However, these findings alone are insufficient to evaluate actual gastric acid-secretory function, and because gastric acid secretion was not directly measured, it remains unclear whether modulation of acid secretion contributed to the gastroprotective effects of PZ. Collectively, the selected 3:1 ginseng–ginger formulation attenuated gastric hemorrhagic lesions, inflammation, and lipid peroxidation while enhancing antioxidant defense in male mice subjected to acute WIRS. These findings may serve as preclinical evidence supporting the potential gastroprotective effects of PZ against acute stress-induced gastric injury. Nevertheless, the present findings do not establish clinical efficacy, safety, an appropriate human intake, or benefits for maintaining gastric health. Evaluation of the clinical applicability of PZ will require validation of its efficacy and safety in longer-term studies and etiologically distinct animal models, followed by pharmacokinetic and bioavailability assessments and appropriately designed clinical trials.