Abstract
Saccharomyces boulardii (S. boulardii) is a probiotic yeast that is widely used to treat gastrointestinal disorders. The present study is aimed to explore the therapeutic effects of S. boulardii on dextran sulfate sodium- (DSS-) induced murine ulcerative colitis (UC) and illustrate the mechanisms of action. C57BL/6 mice were administered S. boulardii (105 and 107 CFU/ml, p.o.) for 3 weeks and then given DSS [2.5% (w/v)] for one week. Administration of S. boulardii prevented DSS-induced reduction in body weight, diarrhea, bloody feces, decreased colon length, and loss of histological structure. Moreover, S. boulardii protected the intestinal barrier by increasing the levels of tight junction proteins zona occludens-1 and Occludin and exerted immunomodulatory effects in DSS-induced mice. Furthermore, S. boulardii suppressed the colonic inflammation by reducing the levels of Interleukin-1β, Interleukin-6, and Tumor necrosis factor alpha and restored myeloperoxidase activity in mice exposed to DSS. S. boulardii also mitigated colonic oxidative damage by increasing the levels of antioxidant enzymes (superoxide dismutase, catalase, and heme oxygenase 1) and glutathione and decreasing malondialdehyde accumulation. Further studies identified that S. boulardii suppressed the nuclear translocation of nuclear factor kappa B (NF-κB) p65 subunit by decreasing IκKα/β levels, while promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) in DSS-exposed mice. Collectively, S. boulardii possessed an appreciable therapeutic effect against the experimental mice model of UC. The protective mechanism of S. boulardii may involve inhibition of NF-κB-mediated proinflammatory signaling and activation of Nrf2-modulated antioxidant defense in addition to intestinal barrier protective and immunomodulatory effects.
Highlights
Ulcerative colitis (UC), one of the inflammatory bowel diseases, is characterized by persistent progression or relapsing inflammation that mainly involves the colonic mucosa and submucosa [1]
S. boulardii suppressed the colonic inflammation by reducing the levels of Interleukin-1β, Interleukin-6, and Tumor necrosis factor alpha and restored myeloperoxidase activity in mice exposed to dextran sodium sulfate (DSS)
Mice exposed to DSS showed significant weight loss from the seventh day (Figure 1(b)), and correspondingly, a notable increase in Disease Activity Index (DAI) (Figure 1(c)) evidenced by apparent diarrhea and rectal bleeding when compared with the control animals
Summary
Ulcerative colitis (UC), one of the inflammatory bowel diseases, is characterized by persistent progression or relapsing inflammation that mainly involves the colonic mucosa and submucosa [1]. As one of the pivotal transcription factors against inflammation and oxidative stress, nuclear factor erythroid 2-related factor 2 (Nrf2) is reported to be implicated in the suppression of proinflammatory signaling and inflammation-associated pathogenesis [11, 12] In this regard, it is likely that NF-κB and Nrf signaling pathways are promising targets for the molecular therapy of UC. Saccharomyces boulardii (S. boulardii) is a probiotic yeast that is resistant to low pH and is highly tolerant to bile acids [13] It has been received more and more attention in the clinical application in recent years due to its beneficial properties including intestinal immune regulation and intestinal barrier protection [14]. The current study was aimed to examine the therapeutic effect of S. boulardii on a well-established mice model of colitis induced by dextran sodium sulfate (DSS) that mimics many clinical symptoms of human UC and, further, investigate the potential mechanisms involved
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