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肝性脑病通过肠-肝-脑轴的肠道微生物组发病机制。

The pathogenesis of gut microbiota in hepatic encephalopathy by the gut-liver-brain axis.

机构信息

Department of Infectious Diseases, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Gene Hospital of Henan Province; Precision Medicine Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

出版信息

Biosci Rep. 2023 Jun 28;43(6). doi: 10.1042/BSR20222524.

DOI:10.1042/BSR20222524
PMID:37279097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10272964/
Abstract

Hepatic encephalopathy (HE) is a neurological disease occurring in patients with hepatic insufficiency and/or portal-systemic blood shunting based on cirrhosis. The pathogenesis is not completely clear till now, but it is believed that hyperammonemia is the core of HE. Hyperammonemia caused by increased sources of ammonia and decreased metabolism further causes mental problems through the gut-liver-brain axis. The vagal pathway also plays a bidirectional role in the axis. Intestinal microorganisms play an important role in the pathogenesis of HE through the gut-liver-brain axis. With the progression of cirrhosis to HE, intestinal microbial composition changes gradually. It shows the decrease of potential beneficial taxa and the overgrowth of potential pathogenic taxa. Changes in gut microbiota may lead to a variety of effects, such as reduced production of short-chain fatty acids (SCFAs), reduced production of bile acids, increased intestinal barrier permeability, and bacterial translocation. The treatment aim of HE is to decrease intestinal ammonia production and intestinal absorption of ammonia. Prebiotics, probiotics, antibiotics, and fecal microbiota transplantation (FMT) can be used to manipulate the gut microbiome to improve hyperammonemia and endotoxemia. Especially the application of FMT, it has become a new treated approach to target microbial composition and function. Therefore, restoring intestinal microbial homeostasis can improve the cognitive impairment of HE, which is a potential treatment method.

摘要

肝性脑病(HE)是发生在肝功能不全和/或门体分流基础上的肝硬化患者的一种神经系统疾病。其发病机制至今尚未完全阐明,但人们认为血氨升高是 HE 的核心。氨的来源增加和代谢减少导致的高氨血症通过肠-肝-脑轴进一步引起精神问题。迷走神经通路在该轴中也发挥双向作用。肠道微生物通过肠-肝-脑轴在 HE 的发病机制中起着重要作用。随着肝硬化向 HE 的进展,肠道微生物组成逐渐发生变化。它表现为潜在有益菌群减少和潜在致病菌群过度生长。肠道微生物群的变化可能导致多种影响,例如短链脂肪酸(SCFA)产生减少、胆汁酸产生减少、肠道屏障通透性增加和细菌易位。HE 的治疗目的是减少肠道氨的产生和氨的肠吸收。可以使用益生元、益生菌、抗生素和粪便微生物移植(FMT)来操纵肠道微生物组,以改善高氨血症和内毒素血症。特别是 FMT 的应用,它已成为一种针对微生物组成和功能的新治疗方法。因此,恢复肠道微生物组平衡可以改善 HE 的认知障碍,这是一种有潜力的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/509a/10272964/7471338c298c/bsr-43-bsr20222524-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/509a/10272964/60b44fde822a/bsr-43-bsr20222524-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/509a/10272964/7471338c298c/bsr-43-bsr20222524-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/509a/10272964/60b44fde822a/bsr-43-bsr20222524-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/509a/10272964/7471338c298c/bsr-43-bsr20222524-g2.jpg

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