Yang Ruipeng, Shan Shuhua, An Ning, Liu Fengming, Cui Kaili, Shi Jiangying, Li Hanqing, Li Zhuoyu
Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan, China.
School of Life Science, Shanxi University, Taiyuan, China.
Front Nutr. 2022 Nov 21;9:1030744. doi: 10.3389/fnut.2022.1030744. eCollection 2022.
Polyphenols from plants possess the anti-inflammatory and gut microbiota modulated properties. Foxtail millet ( L., FM) has potential medical and nutritional functions because of rich phenolic and other phytochemical components.
Here, the study explored the effects of bound polyphenol of inner shell (BPIS) from FM bran on dextran sodium sulfate (DSS)-induced experimental colitis mice.
Results showed that BPIS administration effectively relieved the weight loss, decreased disease active index (DAI) scores, restrained the secretion of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β, increased anti-inflammatory cytokines IL-10, IL-4, IL-5. BPIS prevented gut barrier damage by enhancing tight junction proteins Claudin1, ZO-1 and Occludin, increasing the number of goblet cells and facilitating the gene expressions of mucin family. In addition, BPIS restored the gut microbiota composition and increased the relative abundance of commensal bacteria such as and and restrained the growth of and . Concentrations of short-chain-fatty acids (SCFAs) generated by gut microbiota were elevated in BPIS treated colitis mice.
These data suggest that BPIS effectively ameliorates DSS-induced colitis by preventing intestinal barrier damage and promoting gut microbiota community.
植物多酚具有抗炎和调节肠道微生物群的特性。由于富含酚类和其他植物化学成分,谷子(L.,FM)具有潜在的医学和营养功能。
本研究探讨了谷子麸皮内壳结合多酚(BPIS)对葡聚糖硫酸钠(DSS)诱导的实验性结肠炎小鼠的影响。
结果表明,给予BPIS可有效缓解体重减轻,降低疾病活动指数(DAI)评分,抑制促炎细胞因子TNF-α、IL-6和IL-1β的分泌,增加抗炎细胞因子IL-10、IL-4、IL-5。BPIS通过增强紧密连接蛋白Claudin1、ZO-1和Occludin,增加杯状细胞数量并促进粘蛋白家族的基因表达,防止肠道屏障损伤。此外,BPIS恢复了肠道微生物群组成,增加了共生细菌如和的相对丰度,并抑制了和的生长。在BPIS治疗的结肠炎小鼠中,肠道微生物群产生的短链脂肪酸(SCFAs)浓度升高。
这些数据表明,BPIS通过防止肠道屏障损伤和促进肠道微生物群群落,有效改善了DSS诱导的结肠炎。