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肠道舒缓配方通过调节 NF-κB 信号通路和肠道微生物群减轻了葡聚糖硫酸钠诱导的结肠炎在小鼠中的作用。

Gut relief formula attenuates dextran sulfate sodium-induced colitis by regulating NF-κB signaling and the intestinal microbiota in mice.

机构信息

State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing 100193, China.

Beijing Advanced Innovation Center for Food Nutrition and Human Health, Department of Nutrition and Health, China Agricultural University, Beijing, 100193, China.

出版信息

Food Funct. 2021 Nov 1;12(21):10983-10993. doi: 10.1039/d1fo01477c.

DOI:10.1039/d1fo01477c
PMID:34652352
Abstract

Inflammatory bowel disease (IBD) is a chronic relapsing disorder of the gastrointestinal tract. The nutrition care gut relief formula (GR), a combination of natural products and nutrients, has been shown to benefit gastrointestinal health. However, the underlying mechanism responsible for this effect is incompletely defined. This study was conducted to evaluate the hypothesis that GR could attenuate dextran sulfate sodium (DSS)-induced colitis by enhancing intestinal mucosal immunity and regulating intestinal microflora in mice. Six-week-old C57BL/6J mice orally administered with GR (7.5 mg per mouse per day) or an equal volume of vehicle were treated with sterile water or 2.5% DSS for 6 days to induce colitis. Histological damage, inflammatory cell infiltration, and colonic microbiome community were analyzed to evaluate the beneficial effect of GR. GR administration ameliorated the severity of colitis as evidenced by reduced body weight loss, decreased colon shortening, reduced myeloperoxidase (MPO) activity, inhibited proinflammatory cytokine secretion, and decreased histological damage in DSS-challenged mice. Additionally, enhancement of malondialdehyde (MDA) and hydrogen peroxide (HO) in response to DSS was attenuated by GR administration. Meanwhile, DSS treatment resulted in reduction of the glutathione (GSH) level and tight junction protein abundance, as compared with the controls. Of note, these adverse effects were remarkably eliminated by GR administration. Further study showed that the protective effect of GR was associated with the inhibited activation of STAT3 and NF-κB signaling pathways, as well as upregulated abundances of in the colon tissues of mice. Collectively, the data provided herein demonstrated that GR administration alleviated intestinal mucosal inflammation and mucosal barrier dysfunction. These beneficial effects were associated with inhibited activation of STAT3 and NF-κB signaling pathways, as well as upregulated abundances of in the colon tissues of mice.

摘要

炎症性肠病(IBD)是一种慢性复发性胃肠道疾病。营养保健肠道缓解配方(GR)是一种天然产品和营养素的组合,已被证明有益于胃肠道健康。然而,其作用的潜在机制尚未完全确定。本研究旨在评估以下假设:GR 通过增强肠道黏膜免疫和调节肠道微生物群来减轻葡聚糖硫酸钠(DSS)诱导的结肠炎。6 周龄 C57BL/6J 小鼠口服 GR(每天每只 7.5 毫克)或等量载体,用无菌水或 2.5%DSS 处理 6 天以诱导结肠炎。分析组织学损伤、炎症细胞浸润和结肠微生物群落,以评估 GR 的有益作用。GR 给药改善了结肠炎的严重程度,表现为体重减轻减少、结肠缩短减少、髓过氧化物酶(MPO)活性降低、促炎细胞因子分泌减少和 DSS 攻击小鼠的组织学损伤减少。此外,GR 给药减轻了 DSS 引起的丙二醛(MDA)和过氧化氢(HO)的增加。同时,与对照组相比,DSS 处理导致谷胱甘肽(GSH)水平和紧密连接蛋白丰度降低。值得注意的是,GR 给药显著消除了这些不利影响。进一步的研究表明,GR 的保护作用与抑制 STAT3 和 NF-κB 信号通路的激活以及小鼠结肠组织中 的丰度增加有关。综上所述,本文提供的数据表明,GR 给药减轻了肠道黏膜炎症和黏膜屏障功能障碍。这些有益作用与抑制 STAT3 和 NF-κB 信号通路的激活以及小鼠结肠组织中 的丰度增加有关。

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