Saccharomyces boulardii Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice by Regulating NF-κB and Nrf2 Signaling Pathways.
Saccharomyces boulardii Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice by Regulating NF-κB and Nrf2 Signaling Pathways.
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DOI：
10.1155/2021/1622375
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发表时间：
2021
影响因子：
--
通讯作者：
Yao Y
中科院分区：
文献类型：
--
作者：
Gao H;Li Y;Sun J;Xu H;Wang M;Zuo X;Fu Q;Guo Y;Chen Z;Zhang P;Li X;Wang N;Ye T;Yao Y
布拉酵母（Saccharomyces boulardii）（S.布拉氏菌）是广泛用于治疗胃肠道疾病的益生菌酵母。本研究旨在探讨S.布拉地对葡聚糖硫酸钠（DSS-）诱导的小鼠溃疡性结肠炎（UC）的作用，并说明其作用机制。C57 BL/6小鼠用S.布拉氏菌（105和107 CFU/ml，p.o.）给药3周，然后给予DSS [2.5%（w/v）] 1周。S.布拉地可预防DSS诱导的体重减轻、腹泻、血便、结肠长度缩短和组织结构丧失。此外，S.布拉氏酵母菌通过增加紧密连接蛋白Occludens-1和Occludin的水平来保护肠屏障，并在DSS诱导的小鼠中发挥免疫调节作用。此外，S.布拉地通过降低暴露于DSS的小鼠中白细胞介素-1 β、白细胞介素-6和肿瘤坏死因子α的水平来抑制结肠炎症，并恢复髓过氧化物酶活性。S.布拉地还通过增加抗氧化酶（超氧化物歧化酶、过氧化氢酶和血红素加氧酶1）和谷胱甘肽的水平以及减少丙二醛积累来减轻结肠氧化损伤。进一步的研究表明S.布拉氏酵母菌可通过降低IκKα/β水平抑制核因子κ B（NF-κB）p65亚单位的核转位，而促进核因子红细胞2相关因子2（Nrf 2）的核转位。总的来说，S。布拉地对实验性小鼠UC模型有明显的治疗作用。对S.布拉地可能涉及抑制NF-κ B介导的促炎信号传导和激活Nrf 2调节的抗氧化防御，以及肠屏障保护和免疫调节作用。
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.
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