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Volume 17, Issue 1
  • ISSN: 1874-4672
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Abstract

Ischemia and reperfusion damage to the liver is one of the major causes of hepatic dysfunction and liver failure after a liver transplant. The start of hepatic ischemia-reperfusion damage is linked to metabolic acidosis, Kupffer cells, neutrophils, excessive calcium, and changes in the permeability of the mitochondrial membrane. Hypoxia activates Kupffer cells, resulting in the production of reactive oxygen species (ROS). These ROS when accumulated, causes apoptosis and necrosis, as well as activate immune and inflammatory responses that involve many cells and signalling molecules. Numerous antioxidant compounds have been researched to lessen oxidative stress and thus serve as potential compounds to deal the ischemia-reperfusion damage. This article confers a deep understanding of the protective effects of some effective therapies, including hepatoprotective agents, attenuation of an increase in xanthine oxidase activity, and administration of antioxidants like N-acetylcysteine, superoxide dismutase (SOD), and ornithine.

© 2024 The Author(s). Published by Bentham Science Publisher.
This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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2024-11-23

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/content/journals/cmp/10.2174/1874467217666230803114856
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Hepatic Ischemia-reperfusion Injury: Protective Approaches and Treatment
Curr Mol Pharmacol 17, e030823219400 (2024); https://doi.org/10.2174/1874467217666230803114856
/content/journals/cmp/10.2174/1874467217666230803114856
/content/journals/cmp/10.2174/1874467217666230803114856
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  • Article Type:     Review Article
Keyword(s): Antioxidant; Ischemia preconditioning; Ischemia-reperfusion; N-acetylcysteine; Ornithine; ROS

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