Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKTmTOR Pathways
Joint Authors
Cai, Kailin
Li, Huili
Huang, Kun
Wang, Jiliang
Guo, Jianrong
Zhang, Tao
Gu, Jian
Deng, Xiuling
Chen, Ke
Wang, Guobin
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-18, 18 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-12-13
Country of Publication
Egypt
No. of Pages
18
Main Subjects
Abstract EN
Hepatic ischemia-reperfusion (I/R) injury is a serious complication in patients who have undergone hepatic surgery such as orthotopic liver transplantation and partial hepatectomy.
Recently, a new cytoprotective agent, ursodeoxycholyl lysophosphatidylethanolamide (UDCA-LPE), was reported to protect against hepatic I/R injury.
However, the protective mechanism of UDCA-LPE is not fully understood.
Therefore, we conducted this study to explore its underlying mechanism.
We used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to analyze the liver lipid metabolism changes in mice during I/R.
KEGG enrichment indicated that UDCA-LPE is likely to exert its protective role by regulating fatty acid (FA) metabolism.
Further analysis found that UDCA-LPE significantly increased the ratio of oleic acid (OA) to palmitic acid (PA).
We found that mice pretreated with OA improved tolerance to hepatic I/R injury.
In addition, the phosphorylation level of AKT was markedly upregulated during oxidative stress to promote p65 nuclear translocation, triggering an inflammatory response that exacerbated cell damage and OA treatment significantly inhibited this process.
Notably, OA was found to inhibit H2O2-induced oxidative stress, inflammation, and cell death in HepG2 cells.
Furthermore, we found that OA supplementation to the medium did not result in a significant increase in intracellular OA, but marked increase in the ratio of OA to PA, which may be an important mechanism for the inflammatory response induced by oxidative stress during I/R.
Finally, we demonstrated that OA increased the level of autophagy in HepG2 cells, which may be one of the protective mechanisms against oxidative stress.
Collectively, this study revealed that FA metabolism functionally determines the oxidative stress-related inflammation caused by hepatic I/R.
We hypothesize that OA treatment may be a promising strategy for preventing and treating I/R-induced liver damage.
American Psychological Association (APA)
Guo, Jianrong& Zhang, Tao& Gu, Jian& Cai, Kailin& Deng, Xiuling& Chen, Ke…[et al.]. 2019. Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKTmTOR Pathways. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-18.
https://search.emarefa.net/detail/BIM-1203855
Modern Language Association (MLA)
Guo, Jianrong…[et al.]. Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKTmTOR Pathways. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-18.
https://search.emarefa.net/detail/BIM-1203855
American Medical Association (AMA)
Guo, Jianrong& Zhang, Tao& Gu, Jian& Cai, Kailin& Deng, Xiuling& Chen, Ke…[et al.]. Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKTmTOR Pathways. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-18.
https://search.emarefa.net/detail/BIM-1203855
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203855