紫山药花青素通过选择性促进乳球菌预防脂多糖诱导的肠道损伤

IF 6.9 Q1 FOOD SCIENCE & TECHNOLOGY
Food frontiers Pub Date : 2025-02-25 DOI:10.1002/fft2.546
Pingfei Qiu, Qin Wang, Xiaochun Li, Ruiying Bao, Qingying Cai, ZeRu Peng, LiangMin Huang, Huiyu Shi, Haiwen Zhang, Xuemei Wang
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引用次数: 0

摘要

由于人与猪的生理结构比啮齿类动物具有更高的相似性,因此花青素减轻猪肠道损伤的机制值得进一步探讨。本研究探讨了花青素改善脂多糖诱导的肠道损伤的机制,并通过粪便菌群移植进一步证实了这一机制。将32头仔猪随机分为4组:对照组(control)、模型组(LPS)、预防性花青素组(An-LPS)和预防性粪便微生物群移植组(FMT-LPS)。结果表明,脂多糖诱导的氧化应激增加了空肠p-p65、Bax和Keap1的表达,降低了Nrf2、Occludin和Claudin-1的表达。然而,花青素及其粪便菌群悬浮液逆转了这些影响。同时,花青素选择性地改善某些微生物群,包括乳球菌,导致不同的代谢谱。这些差异有利于激活Nrf2/Keap1等抗氧化相关信号通路,抑制NF-κB等促炎信号通路,从而减轻肠道炎症,显著增加Occludin、Claudin-1等肠道紧密连接蛋白的表达。此外,与LPS相比,An-LPS组血清抗氧化酶活性和IL-10含量均升高。综上所述,花青素通过抗氧化和炎症相关信号通路改善肠道氧化应激;同时,肠道菌群和代谢物在这一过程中起着不可替代的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Purple Yam Anthocyanin Forestalling Lipopolysaccharide-Induced Intestine Damage by Selectively Promoting Lactococcus

Purple Yam Anthocyanin Forestalling Lipopolysaccharide-Induced Intestine Damage by Selectively Promoting Lactococcus

Purple Yam Anthocyanin Forestalling Lipopolysaccharide-Induced Intestine Damage by Selectively Promoting Lactococcus

Purple Yam Anthocyanin Forestalling Lipopolysaccharide-Induced Intestine Damage by Selectively Promoting Lactococcus

Purple Yam Anthocyanin Forestalling Lipopolysaccharide-Induced Intestine Damage by Selectively Promoting Lactococcus

The mechanism of anthocyanin in alleviating intestine injury of pigs is worth pursuing due to the higher similarity of physiological structure between human beings and pigs than rodents. Herein, we investigated the mechanism by which anthocyanin improves gut damage induced with lipopolysaccharide and further confirmed this mechanism using fecal microbiota transplantation. Thirty-two piglets were randomly divided into four treatments: control group (Control), model group (LPS), prophylactic anthocyanin group (An-LPS), and prophylactic fecal microbiota transplantation group (FMT-LPS). The results showed that oxidative stress induced by lipopolysaccharide increased the expression of p-p65, Bax, and Keap1 and decreased the expression of Nrf2, Occludin, and Claudin-1 in jejunum. However, anthocyanin and its fecal microbiota suspension reversed these influences. Meanwhile, anthocyanin selectively improved certain microbiota, including Lactococcus, leading to distinct metabolic profiles. These differences were in favor of activating antioxidant-related signaling pathway, including Nrf2/Keap1 and inhibiting pro-inflammatory signaling pathway such as NF-κB, which alleviated gut inflammation and significantly increased the expression of intestinal tight junction, such as Occludin and Claudin-1. Moreover, compared to LPS, the serum antioxidant enzyme activity and IL-10 content were increased in An-LPS. In conclusion, anthocyanin ameliorated gut oxidative stress through antioxidant- and inflammation-related signaling pathways; meanwhile, gut microbiota and metabolites play a nonsubstitutable role in this process.

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