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Abstract Title:

Liver protective effects of extra virgin olive oil: interaction between its chemical composition and the cell-signaling pathways involved in protection.

Abstract Source:

Endocr Metab Immune Disord Drug Targets. 2017 Nov 14. Epub 2017 Nov 14. PMID: 29141573

Abstract Author(s):

Sandra A Soto-Alarcon, Rodrigo Valenzuela, Alfonso Valenzuela, Luis A Videla

Article Affiliation:

Sandra A Soto-Alarcon

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, whit 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.

Study Type : Review

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Sayer Ji
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