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成熟普洱茶提取物促进肠道微生物群对葡聚糖硫酸钠诱导的结肠炎的恢复力。

Ripened Pu-erh Tea Extract Promotes Gut Microbiota Resilience against Dextran Sulfate Sodium Induced Colitis.

作者信息

Huang Yina, Yang Qin, Mi Xuan, Qiu Liang, Tao Xueying, Zhang Zhihong, Xia Jun, Wu Qinglong, Wei Hua

机构信息

State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, Jiangxi 330031, People's Republic of China.

Wanlongshan Tea Plantation, Pingxiang, Jiangxi 337000, People's Republic of China.

出版信息

J Agric Food Chem. 2021 Feb 24;69(7):2190-2203. doi: 10.1021/acs.jafc.0c07537. Epub 2021 Feb 11.

Abstract

Ripened Pu-erh tea (RPT) has been shown to be an effective natural ingredient to defend against experimentally induced colitis. We hypothesized that RPT would alleviate dextran sulfate sodium (DSS) induced colitis via modulating intestinal microbiota. The effect of RPT on mice gut microbiota was evaluated using 16S rRNA gene amplicon sequencing, broad-spectrum antibiotic (ABX) treatment, and fecal microbiota transplantation (FMT). Pretreatment with RPT enhanced intestinal barrier function, reduced colonic and serum proinflammatory cytokine and macrophage infiltration, and preserved the resilience of gut microbiota in mice during a DSS challenge. Administration of either RPT-regulated or healthy control-derived gut microbiota showed similar protection against colitis, and such protection could not be recapitulated with fecal microbiota from ABX-treated mice, suggesting a key role of protective consortium in the disease protection. Mechanistically, cecal contents of short-chain fatty acids (SCFAs) and colonic peroxisome proliferator activated receptor-γ (PPAR-γ) expression in colitis mice increased significantly by RPT intervention. Collectively, RPT treatment improved DSS-induced colitis by partially reversing the dysbiosis state of gut microbiota, which might be associated with an increase in SCFA level and PPAR-γ expression.

摘要

成熟普洱茶(RPT)已被证明是一种有效的天然成分,可抵御实验性诱导的结肠炎。我们假设RPT可通过调节肠道微生物群来减轻葡聚糖硫酸钠(DSS)诱导的结肠炎。使用16S rRNA基因扩增子测序、广谱抗生素(ABX)治疗和粪便微生物群移植(FMT)评估了RPT对小鼠肠道微生物群的影响。在DSS攻击期间,RPT预处理增强了肠道屏障功能,降低了结肠和血清促炎细胞因子以及巨噬细胞浸润,并维持了小鼠肠道微生物群的恢复力。给予RPT调节的或健康对照来源的肠道微生物群对结肠炎显示出相似的保护作用,而ABX处理小鼠的粪便微生物群无法重现这种保护作用,这表明保护性菌群在疾病保护中起关键作用。从机制上讲,RPT干预显著增加了结肠炎小鼠的盲肠短链脂肪酸(SCFA)含量和结肠过氧化物酶体增殖物激活受体-γ(PPAR-γ)表达。总体而言,RPT治疗通过部分逆转肠道微生物群的失调状态改善了DSS诱导的结肠炎,这可能与SCFA水平和PPAR-γ表达的增加有关。

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