Black chokeberry (Aronia melanocarpa L.) polyphenols attenuate obesity-induced colonic inflammation by regulating gut microbiota and the TLR4/NF-κB signaling pathway in high fat diet-fed rats†

IF 5.1 1区 农林科学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Food & Function Pub Date : 2023-10-06 DOI:10.1039/D3FO02177G
Yue Zhu, Peng-ju Cai, Han-chu Dai, Yu-hang Xiao, Cheng-li Jia and Ai-dong Sun
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引用次数: 1

Abstract

This study investigated the potential benefits of black chokeberry polyphenol (BCP) supplementation on lipopolysaccharide (LPS)-stimulated inflammatory response in RAW264.7 cells and obesity-induced colonic inflammation in a high fat diet (HFD)-fed rat model. Our findings demonstrated that BCP treatment effectively reduced the production of nitric oxide (NO) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and MCP-1) in LPS-induced RAW264.7 cells and concurrently mitigated oxidative stress by modulating the levels of malondialdehyde (MDA), catalase (CAT), and glutathione peroxidase (GSH-Px) in a dose-dependent manner. Furthermore, BCP supplementation significantly ameliorated HFD-induced obesity, improved glucose tolerance, and reduced systemic inflammation in HFD-fed rats. Notably, BCP treatment suppressed the mRNA expression of pro-inflammatory cytokines and alleviated intestinal barrier dysfunction by regulating the mRNA and protein expression of key tight junction proteins (ZO-1, occludin, and claudin-1), thereby inhibiting colonic inflammation caused by the TLR4/NF-κB signaling pathway. Additionally, BCP treatment altered the composition and function of the gut microbiota, leading to an increase in the total content of short-chain fatty acids (SCFAs), particularly acetic acid, propionic acid, isobutyric acid, and butyric acid. Collectively, our results highlighted the potential of BCP supplementation as a promising prebiotic strategy for treating obesity-induced colonic inflammation.

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黑樱桃多酚通过调节高脂饮食喂养大鼠的肠道微生物群和TLR4/NF-κB信号通路,减轻肥胖诱导的结肠炎症。
本研究在高脂饮食(HFD)喂养的大鼠模型中,研究了补充黑樱桃多酚(BCP)对脂多糖(LPS)刺激的RAW264.7细胞炎症反应和肥胖诱导的结肠炎症的潜在益处。我们的研究结果表明,BCP处理有效地减少了LPS诱导的RAW264.7细胞中一氧化氮(NO)和促炎细胞因子(TNF-α、IL-1β、IL-6和MCP-1)的产生,同时通过以剂量依赖的方式调节丙二醛(MDA)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的水平来减轻氧化应激。此外,在HFD喂养的大鼠中,补充BCP显著改善了HFD诱导的肥胖,改善了葡萄糖耐量,并减少了全身炎症。值得注意的是,BCP治疗通过调节关键紧密连接蛋白(ZO-1、occludin和claudin-1)的mRNA和蛋白表达,抑制了促炎细胞因子的mRNA表达,并减轻了肠屏障功能障碍,从而抑制了TLR4/NF-κB信号通路引起的结肠炎症。此外,BCP处理改变了肠道微生物群的组成和功能,导致短链脂肪酸(SCFA)的总含量增加,特别是乙酸、丙酸、异丁酸和丁酸。总之,我们的研究结果强调了补充BCP作为一种治疗肥胖诱导的结肠炎症的有前景的益生元策略的潜力。
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来源期刊
Food & Function
Food & Function BIOCHEMISTRY & MOLECULAR BIOLOGY-FOOD SCIENCE & TECHNOLOGY
CiteScore
10.10
自引率
6.60%
发文量
957
审稿时长
1.8 months
期刊介绍: Food & Function provides a unique venue for physicists, chemists, biochemists, nutritionists and other food scientists to publish work at the interface of the chemistry, physics and biology of food. The journal focuses on food and the functions of food in relation to health.
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