Red Cabbage Juice-Mediated Gut Microbiota Modulation Improves Intestinal Epithelial Homeostasis and Ameliorates Colitis.

Red Cabbage Juice-Mediated Gut Microbiota Modulation Improves Intestinal Epithelial Homeostasis and Ameliorates Colitis.
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红甘蓝汁介导的肠道微生物群调节可改善肠上皮稳态并减轻结肠炎。

DOI:
10.3390/ijms25010539
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发表时间:
2023-12-30
影响因子:
5.6
通讯作者:
Rachagani, Satyanarayana
Rachagani, Satyanarayana
中科院分区:
生物学2区
文献类型:
--
作者:
Wilson, Emily Jean;Natesh, Nagabhishek Sirpu;Ghadermazi, Parsa;Pothuraju, Ramesh;Prajapati, Dipakkumar R.;Pandey, Sanjit;Kaifi, Jussuf T.;Dodam, John R.;Bryan, Jeffrey N.;Lorson, Christian L.;Watrelot, Aude A.;Foster, Jason M.;Mansell, Thomas J.;Chan, Siu Hung Joshua;Batra, Surinder K.;Subbiah, Jeyamkondan;Rachagani, Satyanarayana

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肠道微生物群在炎症性肠病(IBD)中起着至关重要的作用,并且可以通过微生物衍生的代谢物潜在地预防IBD,使其成为一种有前途的治疗途径。最近的证据表明,尽管潜在的机制尚不清楚,但红甘蓝汁(RCJ)可抑制右旋糖酐硫酸钠(DSS)诱导的小鼠结肠炎。因此,该研究旨在揭示RCJ调节肠道微生物群以减轻DSS诱导的小鼠结肠炎的分子机制。使用C57BL/6J小鼠,我们通过两个周期的3%DSS来评估RCJ在DSS诱导的结肠炎中的保护作用。每天用PBS或RCJ管饲小鼠直到终点,并通过鸟枪宏基因组学分析肠道微生物群组成。RCJ治疗显著改善了小鼠的体重(p ≤ 0.001)、存活率(p <0.001)并降低了疾病活动指数(DAI)评分。此外,与DSS组相比,RCJ通过增强RCJ + DSS治疗小鼠中保护性结肠粘蛋白(p <0.001)和紧密连接蛋白(p ≤ 0.01)的表达来改善结肠屏障完整性。鸟枪式宏基因组分析显示,产生短链脂肪酸(SCFAs)的细菌富集(p <0.05),导致过氧化物酶体激活受体γ(PPAR-γ)激活增加(p ≤ 0.001)。这反过来又导致核因子κ B(NF κ B)信号通路的抑制,导致炎性细胞因子和趋化因子的产生减少。我们的研究证明了DSS诱导的小鼠模型中的结肠炎缓解,展示了RCJ作为肠道微生物群和代谢物的潜在调节剂,对IBD的预防和治疗具有重要意义。
Gut microbiota plays a crucial role in inflammatory bowel diseases (IBD) and can potentially prevent IBD through microbial-derived metabolites, making it a promising therapeutic avenue. Recent evidence suggests that despite an unclear underlying mechanism, red cabbage juice (RCJ) alleviates Dextran Sodium Sulfate (DSS)-induced colitis in mice. Thus, the study aims to unravel the molecular mechanism by which RCJ modulates the gut microbiota to alleviate DSS-induced colitis in mice. Using C57BL/6J mice, we evaluated RCJ’s protective role in DSS-induced colitis through two cycles of 3% DSS. Mice were daily gavaged with PBS or RCJ until the endpoint, and gut microbiota composition was analyzed via shotgun metagenomics. RCJ treatment significantly improved body weight (p ≤ 0.001), survival in mice (p < 0.001) and reduced disease activity index (DAI) scores. Further, RCJ improved colonic barrier integrity by enhancing the expression of protective colonic mucins (p < 0.001) and tight junction proteins (p ≤ 0.01) in RCJ + DSS-treated mice compared to the DSS group. Shotgun metagenomic analysis revealed an enrichment of short-chain fatty acids (SCFAs)-producing bacteria (p < 0.05), leading to increased Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) activation (p ≤ 0.001). This, in turn, resulted in repression of the nuclear factor κB (NFκB) signaling pathway, causing decreased production of inflammatory cytokines and chemokines. Our study demonstrates colitis remission in a DSS-induced mouse model, showcasing RCJ as a potential modulator for gut microbiota and metabolites, with promising implications for IBD prevention and treatment.
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