Saccharomyces boulardii Ameliorates Dextran Sulfate Sodium‐Induced Ulcerative Colitis in Mice by Regulating NF‐κB and Nrf2 Signaling Pathways

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.

Efficacy and Safety of Probiotics Combined With Traditional Chinese Medicine for Ulcerative Colitis: A Systematic Review and Meta-Analysis

“…Furthermore, anti-inflammatory cytokines such as IL-10, IL-27 and IL-35 can be expressed and produced by Lactobacillus and non-pathogenic Escherichia coli ( Barra et al, 2020 ). Saccharomyces boulardii can ameliorate DSS-induced colitis in mice by inhibiting the activation of nuclear factor kappa-B (NF-κB) signaling pathway and inhibiting the release of pro-inflammatory cytokines ( Gao et al, 2021 ). Notably, increased short-chain fatty acids generation in response to probiotics can decrease TNF-α and IL-12, increase IL-10, inhibit NF-κB signaling pathway, and produce anti-inflammatory effects ( Säemann et al, 2000 ; Segain, 2000 ).…”

Stronger gut microbiome modulatory effects by postbiotics than probiotics in a mouse colitis model

“…Among the various factors, the role of gut microbiota has received much attention 18 . Moreover, considerable evidence indicates that probiotics administration could attenuate UC-associated symptoms and inflammation, presumably through modulating the gut microbiota (Table 1) [19][20][21][22][23][24][25][26][27][28][29][30][31][32] . Meanwhile, emerging studies also reported that postbiotic application could reduce the risk of development of UC 31,[33][34][35][36] .…”

Effects of Medicinal Plants and Phytochemicals in Nrf2 Pathways during Inflammatory Bowel Diseases and Related Colorectal Cancer: A Comprehensive Review

“…Gao et al [ 182 ] studied Saccharomyces boulardii , a probiotic yeast resistant to low pH and highly tolerant to bile acids, in mice models of UC by regulating the NF-κB and Nrf2 signaling pathways. The authors used a DSS-induced C57BL/6 mice model of colitis and, after treatment with 105 and 107 CFU/mL, p.o.…”