{"title":"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","authors":"Pingfei Qiu, Qin Wang, Xiaochun Li, Ruiying Bao, Qingying Cai, ZeRu Peng, LiangMin Huang, Huiyu Shi, Haiwen Zhang, Xuemei Wang","doi":"10.1002/fft2.546","DOIUrl":null,"url":null,"abstract":"<p>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 <i>Lactococcus</i>, 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.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"6 3","pages":"1439-1453"},"PeriodicalIF":6.9000,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.546","citationCount":"0","resultStr":"{\"title\":\"Purple Yam Anthocyanin Forestalling Lipopolysaccharide-Induced Intestine Damage by Selectively Promoting Lactococcus\",\"authors\":\"Pingfei Qiu, Qin Wang, Xiaochun Li, Ruiying Bao, Qingying Cai, ZeRu Peng, LiangMin Huang, Huiyu Shi, Haiwen Zhang, Xuemei Wang\",\"doi\":\"10.1002/fft2.546\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>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 <i>Lactococcus</i>, 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.</p>\",\"PeriodicalId\":73042,\"journal\":{\"name\":\"Food frontiers\",\"volume\":\"6 3\",\"pages\":\"1439-1453\"},\"PeriodicalIF\":6.9000,\"publicationDate\":\"2025-02-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.546\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Food frontiers\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://iadns.onlinelibrary.wiley.com/doi/10.1002/fft2.546\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"FOOD SCIENCE & TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food frontiers","FirstCategoryId":"1085","ListUrlMain":"https://iadns.onlinelibrary.wiley.com/doi/10.1002/fft2.546","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
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.