Berberine regulates intestinal microbiome and metabolism homeostasis to treat ulcerative colitis

代谢组 阿克曼西亚 拟杆菌 代谢组学 代谢途径 生物 某种肠道细菌 转录组 小檗碱 结肠炎 微生物群 肠道菌群 新陈代谢 药理学 生物化学 基因表达 免疫学 生物信息学 基因 遗传学 细菌
作者
Tao Yang,Niping Qin,Fahui Liu,Yihan Zhao,Wanning Liu,Daiming Fan
出处
期刊:Life Sciences [Elsevier]
卷期号:338: 122385-122385 被引量:23
标识
DOI:10.1016/j.lfs.2023.122385
摘要

This study aims to investigate the effects of berberine (BBR) on the intestinal microbiome (IM) and serum metabolome in ulcerative colitis (UC). Furthermore, the underlying molecular mechanisms of BBR in treating UC also will be explored systematically. A multi-omics approach that integrates the 16s rDNA, serum metabolome, transcriptomics and bioinformatics was profiled to investigate the potential effects of BBR on the IM, serum metabolites and metabolic pathways, and gene expression. In addition, BBR-induced fecal microbiota transplantation (BBR_FMT) was conducted in pseudo germ-free mice combined with the UC model to explore the effects of the IM on metabolic pathways and gene expression. The results of the transcriptomics and metabolic pathway-related genes were further examined by real-time PCR and western blot. BBR ameliorated the community of IM and significantly promoted the abundance of f__Muribaculaceae, Bacteroides, Dubosiella, Allobaculum and Akkermansia. The metabolic profiles in UC mice were significantly modulated by BBR treatment. Furthermore, the inflammation-related metabolites and metabolic pathways in serum were negatively correlated with the abundance of Bacteroides and Akkermansia, which were induced by BBR treatment. BBR_FMT significantly inhibited the arachidonic acid (AA) metabolism pathway and its multiple markers with the mediation of the IM. BBR ameliorated serum metabolic homeostasis by regulating the IM. The inhibition of the AA metabolism pathway and its multiple markers was one of the mechanisms of BBR in the treatment of UC.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
大智若愚啊完成签到,获得积分10
刚刚
刚刚
刚刚
1秒前
1秒前
梅槑发布了新的文献求助10
2秒前
3秒前
3秒前
科研通AI6.3应助zzz采纳,获得10
3秒前
3秒前
Yimi发布了新的文献求助10
4秒前
4秒前
邱宇宸发布了新的文献求助10
4秒前
we发布了新的文献求助10
4秒前
哈哈哈哈h应助D77采纳,获得10
4秒前
4秒前
成功的春梅完成签到,获得积分10
5秒前
苹果花完成签到,获得积分10
5秒前
6秒前
Hao完成签到,获得积分10
6秒前
勤劳的冰淇淋完成签到 ,获得积分10
6秒前
我是老大应助kcl采纳,获得10
6秒前
6秒前
7秒前
OIC发布了新的文献求助10
7秒前
7秒前
8秒前
zhenyan发布了新的文献求助10
8秒前
8秒前
Zhou发布了新的文献求助10
8秒前
zhanghaha发布了新的文献求助10
9秒前
笨笨海秋完成签到,获得积分10
9秒前
织縠完成签到,获得积分10
9秒前
周文瑶发布了新的文献求助10
9秒前
搜集达人应助大气凝云采纳,获得10
9秒前
刻苦剑封完成签到,获得积分10
10秒前
10秒前
大个应助嵩嵩常安采纳,获得10
10秒前
花尽完成签到,获得积分10
10秒前
10秒前
高分求助中
Modern Epidemiology, Fourth Edition 5000
Kinesiophobia : a new view of chronic pain behavior 5000
Molecular Biology of Cancer: Mechanisms, Targets, and Therapeutics 3000
Digital Twins of Advanced Materials Processing 2000
Propeller Design 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
Handbook of pharmaceutical excipients, Ninth edition 1500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 纳米技术 化学工程 生物化学 物理 计算机科学 内科学 复合材料 催化作用 物理化学 光电子学 电极 冶金 细胞生物学 基因
热门帖子
关注 科研通微信公众号,转发送积分 6010478
求助须知:如何正确求助?哪些是违规求助? 7555388
关于积分的说明 16133564
捐赠科研通 5157072
什么是DOI,文献DOI怎么找? 2762231
邀请新用户注册赠送积分活动 1740811
关于科研通互助平台的介绍 1633435