Affiliation:
1. Nutrition Department, Faculty of Medicine, University of Chile, Santiago, Chile
2. Lipid Center, Institute of Nutrition and Food Technology (INTA), Santiago, Chile
3. Molecular and Clinical Pharmacology Program, Institute of Biomedical Science, Faculty of Medicine, University of Chile, Santiago, Chile
Abstract
Background and Objective:
The liver is an organ susceptible to a multitude of injuries that
causes liver damage, like steatosis, non-alcoholic steatohepatitis, cirrhosis, hepatocellular carcinoma,
and ischemia-reperfusion injury. Extra virgin olive oil (EVOO), presents several protective effects on
the liver, reducing hepatic steatosis, hepatocyte ballooning, fibrogenesis, preventing lipid peroxidation,
among other effects. Due to its high levels of monounsaturated fatty acids, mainly oleic acid and phenolic
compounds, such as hydroxytyrosol and oleuropein, EVOO is able to participate in the activation
of different signaling pathways in the hepatocytes involved in the prevention of inflammation, oxidative
stress, endoplasmic reticulum stress, mitochondrial dysfunction, and insulin resistance, allowing
the prevention or resolution of liver damage. The aim of this work is to offer an update of the molecular
effects of EVOO in the liver and its protective properties to prevent the establishment of liver damage
through the regulation of different cell-signaling pathways.
Methods:
Searches that considered the effects of EVOO in in vivo and in vitro models, whith emphasis
in the molecular mechanism of liver tissue damage and prevention and/or treatment of steatosis, steatohepatitis,
cirrhosis, hepatocellular carcinoma, and ischemia-reperfusion injury.
Conclusion:
The most relevant molecular effects of EVOO involved in the prevention or resolution of
liver damage are: (i) Activation of the nuclear transcription factor erythroid-derived 2-like 2 (Nfr2),
inducing the cellular antioxidant response; (ii) Inactivation of the nuclear transcription factor-κB (NF-
κB), preventing the cellular inflammatory response; and (iii) Inhibition of the PERK pathway, preventing
endoplasmic reticulum stress, autophagy, and lipogenic response.
Publisher
Bentham Science Publishers Ltd.
Subject
Immunology and Allergy,Endocrinology, Diabetes and Metabolism