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Bmb6对实验性结肠炎肠道屏障功能的调节作用

Regulatory Effect of Bmb6 on Gut Barrier Functions in Experimental Colitis.

作者信息

Shin Mi-Young, Yong Cheng-Chung, Oh Sejong

机构信息

Microbiology and Functionality Research Group, World Institute of Kimchi, Gwangju 61755, Korea.

Division of Animal Science, Chonnam National University, Gwangju 61186, Korea.

出版信息

Foods. 2020 Jul 2;9(7):864. doi: 10.3390/foods9070864.

Abstract

The integrity of gut barrier functions is closely associated with the pathogenesis of colitis. It is speculated that Bmb6 alleviates colitis by improving the tight junction (TJ) of the inflamed intestinal epithelial layer. In the present study, the regulatory effects of Bmb6 on the TJ barrier to ameliorate colitis-symptoms were investigated. Preliminary screening showed that Bmb6 exhibited strong acid and bile acid tolerance, along with antioxidants and β-galactosidase activities. In a 14-day dextran sulfate sodium (DSS)-induced colitis mouse model, treatment with Bmb6 significantly decreased in the disease activity index score. In addition, histological analyses showed that treatment with Bmb6 protected the structural integrity of the intestinal epithelial layer and mucin-secreting goblet cells from DSS-induced damage, with only slight infiltration of immune cells. Interestingly, western blotting analyses showed that the expression of the TJ protein, zona occluden-1, was restored in Bmb6-treated mice, but not in DSS-induced mice. Consistently, the gene expression of inflammatory cytokines (tumor necrosis factor-α and interferon-γ) was also suppressed in the Bmb6-treated mice. Hence, our findings suggest that suppression of inflammatory conditions enhanced expression of TJ protein, ZO-1, or vice versa, contributing to a colitis-ameliorating effect in Bmb6.

摘要

肠道屏障功能的完整性与结肠炎的发病机制密切相关。据推测,Bmb6通过改善炎症性肠上皮层的紧密连接(TJ)来减轻结肠炎。在本研究中,研究了Bmb6对TJ屏障改善结肠炎症状的调节作用。初步筛选表明,Bmb6表现出较强的耐酸和耐胆汁酸能力,同时具有抗氧化剂和β-半乳糖苷酶活性。在14天右旋糖酐硫酸钠(DSS)诱导的结肠炎小鼠模型中,用Bmb6治疗可显著降低疾病活动指数评分。此外,组织学分析表明,用Bmb6治疗可保护肠上皮层和分泌粘蛋白的杯状细胞的结构完整性免受DSS诱导的损伤,仅有轻微的免疫细胞浸润。有趣的是,蛋白质印迹分析表明,在经Bmb6治疗的小鼠中,TJ蛋白闭合蛋白-1的表达得以恢复,而在DSS诱导的小鼠中则未恢复。同样,在经Bmb6治疗的小鼠中,炎性细胞因子(肿瘤坏死因子-α和干扰素-γ)的基因表达也受到抑制。因此,我们的研究结果表明,抑制炎症条件可增强TJ蛋白ZO-1的表达,反之亦然,这有助于Bmb6产生改善结肠炎的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0297/7404641/f8a741451af1/foods-09-00864-g001.jpg

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