4.7 Article

The role of AMPK-Sirt1-autophagy pathway in the intestinal protection process by propofol against regional ischemia/reperfusion injury in rats

期刊

INTERNATIONAL IMMUNOPHARMACOLOGY
卷 111, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.intimp.2022.109114

关键词

Intestinal injury; AMPK; Sirt1; Autophagy; Propofol

资金

  1. National Natural Science Foundation of China [81873930]
  2. Department of Science and Technology of Sichuan Province [2020YJ0189]
  3. Talent development project of The Affiliated Hospital of SouthwestMedical University [20063]
  4. joint foundation of Luzhou government
  5. Southwest medical university [2021LZXNYD-J28]

向作者/读者索取更多资源

This study investigated the role of the AMPK-Sirt1-autophagy pathway in intestinal injury and found that propofol can reduce intestinal injury and improve the prognosis by activating this pathway.
Intestinal ischemia/reperfusion (II/R) is a clinical event associated with high morbidity and mortality. AMP -activated protein kinase (AMPK), a central cellular energy sensor, is associated with oxidative stress and inflammation. However, whether the AMPK is involved in the II/R-induced intestinal injury and the underlying mechanism is yet to be elucidated. Propofol has a protective effect on organs; yet, its specific mechanism of action remains unclear. This study explored the role of the AMPK-Sirt1-autophagy pathway in intestinal injury, and whether propofol could reduce intestinal injury and investigated the mechanisms in a rat model of II/R injury as well as a cell model (IEC-6 cells) of hypoxia/reoxygenation (H/R). Propofol, AMPK agonist (AICAR) and AMPK inhibitor (Compound C) were then administered, respectively. The histopathological changes, cell viability and apoptosis were detected. Furthermore, the levels of proinflammatory factors, the activities of oxidative stress, diamine oxidase, and signaling pathway were also analyzed. The results demonstrated that the AMPK-Sirt1-autophagy pathway of intestine was activated after II/R or H/R. Propofol could further activate the pathway, which reduced intestinal injury, inhibited apoptosis, reversed inflammation and oxidative stress, and improved the 24-hour survival rate in II/R rats in vivo, and attenuated H/R-induced IEC-6 cell injury, oxidative stress, and apoptosis in vitro, as fine as changes in AICAR treatment. Compound C abrogated the protective effect of propofol on II/R and H/R-induced injury. These results suggested a crucial effect of AMPK on the mechanism of intestinal injury and might provide a new insight into the mechanism of propofol reducing II/R injury.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据