Varela-Mendoza Atziri A, Martínez-Flores Ma Magdalena, Paz-Jiménez Melanie G, García-Acevedo Fernanda, Córdova-Dávalos Laura E, Barrios-García Tonatiuh, Martínez-Saldaña Ma Consolación, Salinas-Guardado Valeria, Jiménez Mariela, Salinas Eva, Cervantes-García Daniel
Department of Microbiology, Basic Science Center Autonomous University of Aguascalientes Aguascalientes Mexico.
Department of Morphology, Basic Science Center Autonomous University of Aguascalientes Aguascalientes Mexico.
Food Sci Nutr. 2025 Aug 16;13(8):e70804. doi: 10.1002/fsn3.70804. eCollection 2025 Aug.
Kombucha is a fermented beverage with high contents of antioxidants and probiotics. Enteric damage due to uncontrolled consumption of non-steroidal anti-inflammatory drugs (NSAIDs) represents a significant cause of morbidity and mortality. This study aimed to evaluate the preventive effects of kombucha against indomethacin-induced enteric damage. Wistar rats were divided into control (Ctrl), supplemented with kombucha (Komb), indomethacin-induced enteric damage (Indo), and indomethacin-induced enteric damage and supplemented with kombucha (Indo-Komb) groups. We analyzed ulcer index, histological changes, gene expression of intestinal barrier function genes, and microbiota phyla in cecal content. Kombucha supplementation reduced ulcer index and intestinal inflammation, which improved survival ( = 0.0291), maintained body weight, ( < 0.001) and avoided the drop in levels of hemoglobin, hematocrit, and erythrocytes ( < 0.001). Histopathological analyses of intestines revealed impaired integrity of villi with inflammatory infiltrates, which were significantly prevented with kombucha supplementation ( = 0.0024 and = 0.0017, respectively). Rats that received kombucha upregulated the expression of tight junction genes , , and ( = 0.027, = 0.024, < 0.001, respectively). The upregulation of the oxidative and inflammatory markers , , and was prevented by kombucha intake ( < 0.001). Additionally, kombucha ameliorated the dysbiosis in indomethacin-induced enteric damaged rats by reduction of ( < 0.001) while increasing abundance. This study demonstrated that kombucha consumption is a viable strategy to delay NSAID-induced enteric damage through enhancement of intestinal barrier integrity and prevention of dysbiosis.
康普茶是一种富含抗氧化剂和益生菌的发酵饮料。非甾体抗炎药（NSAIDs）无节制消费导致的肠道损伤是发病和死亡的一个重要原因。本研究旨在评估康普茶对吲哚美辛诱导的肠道损伤的预防作用。将Wistar大鼠分为对照组（Ctrl）、补充康普茶组（Komb）、吲哚美辛诱导的肠道损伤组（Indo）和吲哚美辛诱导的肠道损伤并补充康普茶组（Indo-Komb）。我们分析了溃疡指数、组织学变化、肠道屏障功能基因的基因表达以及盲肠内容物中的微生物门类。补充康普茶可降低溃疡指数和肠道炎症，从而提高存活率（P = 0.0291），维持体重（P < 0.001），并避免血红蛋白、血细胞比容和红细胞水平下降（P < 0.001）。肠道组织病理学分析显示绒毛完整性受损并有炎性浸润，补充康普茶可显著预防这些情况（分别为P = 0.0024和P = 0.0017）。接受康普茶的大鼠上调了紧密连接基因、和的表达（分别为P = 0.027、P = 0.024、P < 0.001）。康普茶摄入可防止氧化和炎症标志物、和的上调（P < 0.001）。此外，康普茶通过降低（P < 0.001）同时增加丰度来改善吲哚美辛诱导的肠道损伤大鼠的菌群失调。本研究表明，饮用康普茶是一种可行的策略，可通过增强肠道屏障完整性和预防菌群失调来延缓NSAIDs诱导的肠道损伤。
