State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
College of Cooking Science and Technology, Jiangsu College of Tourism, Yangzhou 225000, China.
Food Funct. 2021 Oct 4;12(19):8976-8993. doi: 10.1039/d1fo01446c.
Ulcerative colitis (UC) is one of the most prevalent inflammatory bowel diseases (IBD) worldwide, while oat β-glucan has been shown to suppress the progress of colitis in UC mice. However, the underlying mechanism of oat β-glucan in ameliorating colitis is unclear and the role of gut microbiota in the protective effect of oat β-glucan against colitis remains unknown. In the present study, we aim to investigate the effect of oat β-glucan on gut microbiota in colitis mice and explore the health effect related mechanism. Dextran sulfate sodium (DSS) was used to induce the colitis model in mice. The results showed that β-glucan treatment attenuated hematochezia, splenomegaly and colon shortening in colitis mice. Histological evaluation of H&E and TUNEL staining showed that β-glucan treatment suppressed DSS-induced colonic inflammatory infiltration and reduced cell apoptosis levels of colon tissues. mRNA expression levels of the pro-inflammatory factors were also significantly reduced in the β-glucan group. Moreover, β-glucan treatment increased the protein and mRNA expression levels of tight junction proteins. Analysis of gut microbiota community showed that β-glucan treatment modulated gut microbial composition and structure at the OTU level in colitis mice. Further analysis of gut microbial metabolism revealed that β-glucan treatment significantly increased acetate, propionate and butyrate concentrations, and affected microbial metabolome in colitis mice. Notably, the increased acetate and propionate concentrations could directly affect pro-inflammatory factor expression levels and tight junction protein levels. In contrast, the changes in metabolic profiles affected pro-inflammatory factor levels and thus affected tight junction protein levels. Overall, our study revealed that oat β-glucan ameliorated DSS-induced colitis in mice simultaneously through regulating gut-derived short-chain fatty acids (SCFAs) and microbial metabolic biomarkers. Our study demonstrated that oat β-glucan could be an effective nutritional intervention strategy towards targeting gut microbiota metabolism for ameliorating colitis.
溃疡性结肠炎（UC）是全球最常见的炎症性肠病（IBD）之一，而燕麦β-葡聚糖已被证明可抑制 UC 小鼠的结肠炎进展。然而，燕麦β-葡聚糖改善结肠炎的潜在机制尚不清楚，肠道微生物群在燕麦β-葡聚糖对结肠炎的保护作用中的作用也尚不清楚。在本研究中，我们旨在研究燕麦β-葡聚糖对结肠炎小鼠肠道微生物群的影响，并探索其与健康相关的作用机制。我们使用葡聚糖硫酸钠（DSS）诱导小鼠结肠炎模型。结果表明，β-葡聚糖治疗可减轻结肠炎小鼠的血便、脾肿大和结肠缩短。H&E 和 TUNEL 染色的组织学评估表明，β-葡聚糖治疗可抑制 DSS 诱导的结肠炎症浸润并降低结肠组织的细胞凋亡水平。β-葡聚糖组中促炎因子的 mRNA 表达水平也显著降低。此外，β-葡聚糖治疗可增加紧密连接蛋白的蛋白和 mRNA 表达水平。肠道微生物群落分析表明，β-葡聚糖治疗可调节结肠炎小鼠的肠道微生物组成和结构在 OTU 水平上。对肠道微生物代谢的进一步分析表明，β-葡聚糖治疗可显著增加乙酸盐、丙酸盐和丁酸盐的浓度，并影响结肠炎小鼠的微生物代谢组。值得注意的是，增加的乙酸盐和丙酸盐浓度可以直接影响促炎因子表达水平和紧密连接蛋白水平。相反，代谢谱的变化影响了促炎因子水平，从而影响了紧密连接蛋白水平。总的来说，我们的研究表明，燕麦β-葡聚糖通过调节肠道来源的短链脂肪酸（SCFAs）和微生物代谢生物标志物，同时改善 DSS 诱导的结肠炎小鼠。我们的研究表明，燕麦β-葡聚糖可以作为一种有效的营养干预策略，针对肠道微生物群代谢来改善结肠炎。
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