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木耳甘油酯通过减轻炎症反应、氧化应激和核因子κB的表达来保护肝脏免受缺血/再灌注损伤。

Agaricoglycerides Protect against Hepatic Ischemia/Reperfusion Injury by Attenuating Inflammatory Response, Oxidative Stress, and Expression of NF-κB.

作者信息

Zhao Xiang-Qian, Liang Bin, Liu Yang, Huang Xiao-Qiang

机构信息

Hospital & Institute of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing 100853, China.

出版信息

Evid Based Complement Alternat Med. 2015;2015:142736. doi: 10.1155/2015/142736. Epub 2015 Apr 16.

DOI:10.1155/2015/142736
PMID:25960746
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4415680/
Abstract

We have investigated the effects of agaricoglycerides (AG) in a mouse model of hepatic I/R injury. I/R triggered increases/changes in markers of liver injury, hepatic oxidative stress, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and nuclear factor κB (NF-κB). AG significantly reduced the extent of liver inflammation and oxidative stress and also attenuated the NF-κB activation as well as TNF-α and IL-1β production. Our results indicate that AG may represent a novel protective strategy against I/R-induced injury and inflammatory diseases.

摘要

我们在小鼠肝缺血/再灌注损伤模型中研究了木耳甘油酯（AG）的作用。缺血/再灌注引发了肝损伤、肝氧化应激、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和核因子κB（NF-κB）标志物的增加/变化。AG显著降低了肝脏炎症和氧化应激的程度，还减弱了NF-κB的激活以及TNF-α和IL-1β的产生。我们的结果表明，AG可能代表一种针对缺血/再灌注诱导的损伤和炎症性疾病的新型保护策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/89f602336923/ECAM2015-142736.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/dfc6490f2457/ECAM2015-142736.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/c9341d5a1cb7/ECAM2015-142736.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/be9895b937cf/ECAM2015-142736.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/ddc3e24d1c70/ECAM2015-142736.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/89f602336923/ECAM2015-142736.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/dfc6490f2457/ECAM2015-142736.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/160160cba00e/ECAM2015-142736.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/c9341d5a1cb7/ECAM2015-142736.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/be9895b937cf/ECAM2015-142736.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314b/4415680/89f602336923/ECAM2015-142736.006.jpg

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Oxidative inactivation of key mitochondrial proteins leads to dysfunction and injury in hepatic ischemia reperfusion.
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