Gastritis refers to inflammation caused by injury to the gastric epithelium, which is usually due to excessive alcohol consumption and prolonged use of nonsteroidal anti‑inflammatory drugs. Millions of individuals worldwide suffer from this disease. However, the lack of safe and promising treatments makes it urgent to explore and develop leads from natural resources. Therefore, food as medicine may be the best approach for the treatment of these disorders. The present study described the protective effects of food‑polydeoxyribonucleotides (f‑PDRNs) in a rat model of gastric mucosal injury induced by HCl‑EtOH. Administration of f‑PDRN was performed with low‑PRF002 (26 mg/kg/day), medium‑PRF002 (52 mg/kg/day) and high‑PRF002 (78 mg/kg/day) on the day of autopsy. The site of damage to the mucous membrane was also analysed. In addition, an increase in gastric juice pH, total acidity of gastric juice and decrease in gastric juice secretion were confirmed, and gastric juice secretion‑related factors corresponding to the administration of f‑PDRN were analysed. Administration of f‑PDRN reduced the mRNA expression of histamine H2 receptor, muscarinic acetylcholine receptor M3, cholecystokinin 2 receptor and H⁺/K⁺ ATPase related to gastric acid secretion and downregulation of histamine, myeloperoxidase and cyclic adenosine monophosphate. In addition, it was histologically confirmed that the loss of epithelial cells and the distortion of the mucosa were recovered in the group in which f‑PDRN was administered compared to the model group with gastric mucosa damage. In summary, the present study suggested that f‑PDRN has therapeutic potential and may have beneficial effects if taken regularly as a food supplement.

中文翻译：

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通过口服食物聚脱氧核糖核苷酸改善酒精引起的胃粘膜损伤。

胃炎是指胃上皮损伤引起的炎症，通常是由于过量饮酒和长期使用非甾体类抗炎药所致。全世界有数百万人患有这种疾病。然而，由于缺乏安全和有希望的治疗方法，因此迫切需要从自然资源中探索和开发线索。因此，食物作为药物可能是治疗这些疾病的最佳方法。本研究描述了食物-聚脱氧核糖核苷酸 (f-PDRN) 在 HCl-EtOH 诱导的大鼠胃黏膜损伤模型中的保护作用。在尸检当天，使用低-PRF002（26 mg/kg/天）、中等-PRF002（52 mg/kg/天）和高-PRF002（78 mg/kg/天）进行了f-PDRN给药。还分析了对粘膜的损伤部位。此外，证实了胃液pH值、胃液总酸度和胃液分泌减少，并分析了与给予f-PDRN相对应的胃液分泌相关因素。f-PDRN 的给药降低了组胺 H2 受体、毒蕈碱乙酰胆碱受体 M3、胆囊收缩素 2 受体和 H 的 mRNA 表达⁺ /K ⁺ ATPase 与胃酸分泌和组胺、髓过氧化物酶和环磷酸腺苷的下调有关。此外，组织学证实，与胃黏膜损伤模型组相比，f-PDRN给药组上皮细胞丢失和黏膜变形恢复。总之，本研究表明 f-PDRN 具有治疗潜力，如果定期作为食品补充剂服用，可能会产生有益效果。