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甜茶通过调节肠道微生物群和丁酸介导的抗炎信号预防小鼠溃疡性结肠炎。

Prevention of Ulcerative Colitis in Mice by Sweet Tea () via the Regulation of Gut Microbiota and Butyric-Acid-Mediated Anti-Inflammatory Signaling.

机构信息

Research Center for Plants and Human Health, Institute of Urban Agriculture, Chinese Academy of Agricultural Sciences, Chengdu National Agricultural Science & Technology Center, Chengdu 610213, China.

Key Laboratory of Coarse Cereal Processing (Ministry of Agriculture and Rural Affairs), Sichuan Engineering & Technology Research Center of Coarse Cereal Industralization, School of Food and Biological Engineering, Chengdu University, Chengdu 610106, China.

出版信息

Nutrients. 2022 May 26;14(11):2208. doi: 10.3390/nu14112208.

DOI:10.3390/nu14112208
PMID:35684007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9183097/
Abstract

Sweet tea ( [Hance] Chun) is a new resource for food raw materials, with plenty of health functions. This study aimed to investigate the preventive effect and potential mechanism of sweet tea extract (STE) against ulcerative colitis (UC). Briefly, BABL/c mice were treated with STE (100 and 400 mg/kg) for 2 weeks to prevent 3% dextran sulfate sodium (DSS)-induced UC. It was found that STE supplementation significantly prevented DSS-induced UC symptoms; suppressed the levels of pro-inflammatory mediators, such as myeloperoxidase and tumor necrosis factor-α; increased the levels of anti-inflammatory cytokines; and up-regulated the expression of tight junction proteins (Zonula occludens-1 and Occludin). STE also altered the gut microbiota profile of UC mice by increasing , , , _NK4A136_group, and and inhibiting , , and , accompanied by a significant increase in the content of butyric acid. Moreover, STE increased the expression of G-protein-coupled receptor (GPR) 43 and GPR109A and inhibited the expression of histone deacetylase 3 (HDAC3) and nuclear factor-κB p65 (NF-κB p65) in the colon. In conclusion, this study indicated that STE has a good preventive effect on UC by regulating gut microbiota to activate butyrate-GPR-mediated anti-inflammatory signaling and simultaneously inhibit HDAC3/NF-κB inflammatory signaling.

摘要

甜茶（[Hance] Chun）是一种新的食品原料资源，具有丰富的健康功能。本研究旨在探讨甜茶提取物（STE）对溃疡性结肠炎（UC）的预防作用及潜在机制。简要地说，BABL/c 小鼠用 STE（100 和 400mg/kg）处理 2 周，以预防 3%葡聚糖硫酸钠（DSS）诱导的 UC。结果发现，STE 补充剂能显著预防 DSS 诱导的 UC 症状；抑制促炎介质如髓过氧化物酶和肿瘤坏死因子-α的水平；增加抗炎细胞因子的水平；并上调紧密连接蛋白（闭锁蛋白-1 和 Occludin）的表达。STE 还通过增加、、、NK4A136 组、和、抑制、和、来改变 UC 小鼠的肠道微生物群谱，伴随着丁酸含量的显著增加。此外，STE 增加了 G 蛋白偶联受体（GPR）43 和 GPR109A 的表达，抑制了结肠中组蛋白去乙酰化酶 3（HDAC3）和核因子-κB p65（NF-κB p65）的表达。总之，本研究表明，STE 通过调节肠道微生物群来激活丁酸盐-GPR 介导的抗炎信号，同时抑制 HDAC3/NF-κB 炎症信号，对 UC 具有良好的预防作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/1b0cf78fc8c3/nutrients-14-02208-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/3a998a94711e/nutrients-14-02208-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/2d1dc614799e/nutrients-14-02208-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/264841288c5f/nutrients-14-02208-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/f13af85bd890/nutrients-14-02208-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/1162c1ca80f4/nutrients-14-02208-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/9a2e4842a15c/nutrients-14-02208-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/1b0cf78fc8c3/nutrients-14-02208-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/3a998a94711e/nutrients-14-02208-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/2d1dc614799e/nutrients-14-02208-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/264841288c5f/nutrients-14-02208-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/f13af85bd890/nutrients-14-02208-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/1162c1ca80f4/nutrients-14-02208-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/9a2e4842a15c/nutrients-14-02208-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d1f/9183097/1b0cf78fc8c3/nutrients-14-02208-g007.jpg

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[2]
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[3]
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[4]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Jellyfish skin polysaccharides enhance intestinal barrier function and modulate the gut microbiota in mice with DSS-induced colitis.

Food Funct. 2021-10-19

[2]
Vitamin A supplementation ameliorates ulcerative colitis in gut microbiota-dependent manner.

Food Res Int. 2021-10

[3]
Phenolic Content, Main Flavonoids, and Antioxidant Capacity of Instant Sweet Tea ( [Hance] Chun) Prepared with Different Raw Materials and Drying Methods.

Foods. 2021-8-19

[4]
Protective Effect of the Flower Extract on DSS-Induced Ulcerative Colitis in Mice.

Evid Based Complement Alternat Med. 2021-8-9

[5]
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Anneslea fragrans Wall. ameliorates ulcerative colitis via inhibiting NF-κB and MAPK activation and mediating intestinal barrier integrity.

J Ethnopharmacol. 2021-10-5

[7]
Acrylamide exposure aggravates the development of ulcerative colitis in mice through activation of NF-κB, inflammatory cytokines, iNOS, and oxidative stress.

Iran J Basic Med Sci. 2021-3

[8]
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Food Funct. 2021-6-8

[9]
Effect of Trilobatin from Rehd on Gut Microbiota of Obese Rats Induced by a High-Fat Diet.

Nutrients. 2021-3-10

[10]
Lychee ( Sonn.) Pulp Phenolics Activate the Short-Chain Fatty Acid-Free Fatty Acid Receptor Anti-inflammatory Pathway by Regulating Microbiota and Mitigate Intestinal Barrier Damage in Dextran Sulfate Sodium-Induced Colitis in Mice.

J Agric Food Chem. 2021-3-24

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