Oleuropein As a Therapeutic Agent for Non-Alcoholic Fatty Liver Disease During Hepatitis C Publisher



Sotoudeheian M¹ ; Hoseini SA² ; Mirahmadi SMS³ ; Farahmandian N⁴ ; Pazokitoroudi H¹ Show Affiliations
Source: Revista Brasileira de Farmacognosia Published:2023

Abstract

Hepatitis C is defined as an infection of hepatocytes by the hepatitis C virus that affects hepatocellular signaling pathways and can lead to non-alcoholic fatty liver disease. In this manuscript, an herbal therapeutic agent is proposed for the treatment of non-alcoholic fatty liver disease caused by hepatitis C virus infection. Adenosine monophosphate–activated protein kinase, extracellular signal–regulated kinase, peroxisome proliferator–activated receptors, mammalian target of rapamycin, and autophagy cascades are among the signaling pathways thought to be involved in this hepatocellular event. Oleuropein has been shown to be effective in the treatment of this liver condition. Overall, our study demonstrated that peroxisome proliferator–activated receptors α and peroxisome proliferator–activated receptors γ signaling pathways regulate hepatic steatosis via triacylglyceride homeostasis. Consequently, triacylglyceride content in hepatocytes modulates autophagy. The modulation of autophagy in hepatic steatosis may be a consequence of the response of the adenosine monophosphate–activated protein kinase pathway to excessive hepatic fat accumulation in hepatitis C. Oleuropein affects peroxisome proliferator–activated receptors and adenosine monophosphate–activated protein kinase signaling during hepatitis C virus infection, regulates extracellular signal–regulated kinase and autophagy, and modulates autophagy-associated steatosis. In addition, oleuropein reduced the expression of some liver genes involved in oxidative stress response, detoxification of lipid peroxidation products, and proinflammatory cytokine genes. Thus, oleuropein is involved in lipogenesis, inflammation, and insulin resistance and has a beneficial effect on hepatitis C induced by non-alcoholic fatty liver disease. Graphical Abstract: [Figure not available: see fulltext.]. © 2023, The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia.