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Published on: January 5, 2017
Kombucha Prevents Indomethacin-Induced Enteric Damage in Wistar Rat by Enhancing Epithelial Gut Barrier and
Atziri A Varela-Mendoza1, Ma Magdalena Martínez-Flores1, Melanie G Paz-Jiménez1
1Department of Microbiology, Basic Science Center Autonomous University of Aguascalientes Aguascalientes Mexico.
Abstract:
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 (p = 0.0291), maintained body weight, (p < 0.001) and avoided the drop in levels of hemoglobin, hematocrit, and erythrocytes (p < 0.001). Histopathological analyses of intestines revealed impaired integrity of villi with inflammatory infiltrates, which were significantly prevented with kombucha supplementation (p = 0.0024 and p = 0.0017, respectively). Rats that received kombucha upregulated the expression of tight junction genes Muc2, Cldn1, and Ocln (p = 0.027, p = 0.024, p < 0.001, respectively). The upregulation of the oxidative and inflammatory markers Nos2, Mpo, and Tnf was prevented by kombucha intake (p < 0.001). Additionally, kombucha ameliorated the dysbiosis in indomethacin-induced enteric damaged rats by reduction of Proteobacteria (p < 0.001) while increasing Firmicutes 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.

