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肠道缺血再灌注诱导急性肝损伤的相关机制

Mechanism Involved in Acute Liver Injury Induced by Intestinal Ischemia-Reperfusion.

作者信息

Jin Binghui, Li Guangyao, Zhou Lin, Fan Zhe

机构信息

Department of General Surgery, The Third People's Hospital of Dalian, Dalian Medical University, Dalian, China.

Department of Central Laboratory, The Third People's Hospital of Dalian, Dalian Medical University, Dalian, China.

出版信息

Front Pharmacol. 2022 May 23;13:924695. doi: 10.3389/fphar.2022.924695. eCollection 2022.

DOI:10.3389/fphar.2022.924695
PMID:35694264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9185410/
Abstract

Intestinal ischemia-reperfusion (I/R) is a common pathophysiological process, which can occur in many conditions such as acute enteric ischemia, severe burns, small intestinal transplantation, etc,. Ischemia-reperfusion of the intestine is often accompanied by distal organ injury, especially liver injury. This paper outlined the signal pathways and cytokines involved in acute liver injury induced by intestinal I/R: the NF-κB Signaling Pathway, the P66shc Signaling Pathway, the HMGB1 Signaling Pathway, the Nrf2-ARE Signaling Pathway, the AMPK-SIRT-1 Signaling Pathway and other cytokines, providing new ideas for the prevention and treatment of liver injury caused by reperfusion after intestinal I/R.

摘要

肠缺血再灌注（I/R）是一种常见的病理生理过程，可发生于多种情况，如急性肠道缺血、严重烧伤、小肠移植等。肠道缺血再灌注常伴有远端器官损伤，尤其是肝损伤。本文概述了肠I/R诱导的急性肝损伤所涉及的信号通路和细胞因子：核因子κB信号通路、P66shc信号通路、高迁移率族蛋白B1信号通路、核因子E2相关因子2-抗氧化反应元件信号通路、腺苷酸活化蛋白激酶-沉默信息调节因子1信号通路以及其他细胞因子，为预防和治疗肠I/R后再灌注引起的肝损伤提供了新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/81339f2aa8b5/fphar-13-924695-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/749e9b938ffd/fphar-13-924695-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/49dbb05fb1d1/fphar-13-924695-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/1333d4f66d7f/fphar-13-924695-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/d4947bc946c2/fphar-13-924695-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/81339f2aa8b5/fphar-13-924695-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/749e9b938ffd/fphar-13-924695-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/49dbb05fb1d1/fphar-13-924695-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/1333d4f66d7f/fphar-13-924695-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/d4947bc946c2/fphar-13-924695-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/9185410/81339f2aa8b5/fphar-13-924695-g005.jpg

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