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用乙醛脱氢酶2（ALDH2）激动剂Alda-1进行预处理可减轻小鼠缺血再灌注诱导的肠道损伤。

Pretreatment with the ALDH2 agonist Alda-1 reduces intestinal injury induced by ischaemia and reperfusion in mice.

作者信息

Zhu Qiankun, He Guizhen, Wang Jie, Wang Yukang, Chen Wei

机构信息

Department of Parenteral and Enteral Nutrition, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, 100730, China.

Department of Parenteral and Enteral Nutrition, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, 100730, China

出版信息

Clin Sci (Lond). 2017 Jun 1;131(11):1123-1136. doi: 10.1042/CS20170074. Epub 2017 Mar 21.

DOI:10.1042/CS20170074
PMID:28325855
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5434792/
Abstract

Many studies demonstrate that activation of aldehyde dehydrogenase 2 (ALDH2) protects against oxidative stress via detoxification of cytotoxic aldehydes, and could attenuate cardiac, cerebral, lung and renal ischaemia-reperfusion (I/R) injuries. However, the effect of ALDH2 in intestinal I/R is unknown. The present study was set up to determine whether an ALDH2 agonist, Alda-1, could alleviate intestinal injury after gut I/R. In a mouse model of intestinal I/R injury, histological grading, proinflammatory cytokines, oxidative stress, cellular apoptosis, chemokine contents, ALDH2 activity, 4-hydroxy--2-nonenal (4-HNE) and malondialdehyde (MDA) were evaluated. The results indicated that I/R treatment conferred elevation in pathological scores, proinflammatory cytokines, oxidative stress, cellular apoptosis and chemokine levels, accompanied by accumulated 4-HNE and MDA. No significant changes in ALDH2 activity were observed after I/R. However, Alda-1 pretreatment significantly decreased these injurious indicators, concomitant with up-regulated ALDH2 activity, and lessened 4-HNE and MDA accumulation. Taken together, our results implicate activation of ALDH2 by Alda-1 in the significant abatement intestinal I/R injury.

摘要

许多研究表明，醛脱氢酶2（ALDH2）的激活通过对细胞毒性醛的解毒作用来抵御氧化应激，并可减轻心脏、脑、肺和肾的缺血再灌注（I/R）损伤。然而，ALDH2在肠道I/R中的作用尚不清楚。本研究旨在确定一种ALDH2激动剂Alda-1是否能减轻肠道I/R后的肠道损伤。在肠道I/R损伤的小鼠模型中，评估了组织学分级、促炎细胞因子、氧化应激、细胞凋亡、趋化因子含量、ALDH2活性、4-羟基-2-壬烯醛（4-HNE）和丙二醛（MDA）。结果表明，I/R处理导致病理评分、促炎细胞因子、氧化应激、细胞凋亡和趋化因子水平升高，同时伴有4-HNE和MDA的积累。I/R后未观察到ALDH2活性有显著变化。然而，Alda-1预处理显著降低了这些损伤指标，同时上调了ALDH2活性，并减少了4-HNE和MDA的积累。综上所述，我们的结果表明Alda-1激活ALDH2可显著减轻肠道I/R损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da00/5434792/b543567bf3f7/cs1311123fig8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da00/5434792/b543567bf3f7/cs1311123fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da00/5434792/deef01385270/cs1311123fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da00/5434792/f687a1239e6e/cs1311123fig2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da00/5434792/b543567bf3f7/cs1311123fig8.jpg

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