Abstract

Background/objectiveZingiber officinale Roscoe (ginger) (Zingiberaceae) has been cultivated for thousands of years both as a spice and for medicinal purposes. Ginger rhizomes successive extracts (petroleum ether, chloroform and ethanol) were examined against liver fibrosis induced by carbon tetrachloride in rats.ResultsThe evaluation was done through measuring antioxidant parameters; glutathione (GSH), total superoxide dismutase (SOD) and malondialdehyde (MDA). Liver marker enzymes; succinate and lactate dehydrogenases (SDH and LDH), glucose-6-phosphatase (G-6-Pase), acid phosphatase (AP), 5'- nucleotidase (5'NT) and liver function enzymes; aspartate and alanine aminotransferases (AST and ALT) as well as cholestatic markers; alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total bilirubin were estimated. Liver histopathological analysis and collagen content were also evaluated. Treatments with the selected extracts significantly increased GSH, SOD, SDH, LDH, G-6-Pase, AP and 5'NT. However, MDA, AST, ALT ALP, GGT and total bilirubin were significantly decreased.ConclusionsExtracts of ginger, particularly the ethanol one resulted in an attractive candidate for the treatment of liver fibrosis induced by CCl4. Further studies are required in order to identify the molecules responsible of the pharmacological activity.

Highlights

  • Liver plays a pivotal role in regulating various physiological processes in the body such as metabolism, secretion and storage

  • Evidences developed over the last years have suggested that various forms of liver injuries may be caused by free radical formation and subsequent oxidative stress

  • Oxidative stress lead to the formation of glycoxidation products, including advanced glycation end products

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Summary

Introduction

Liver plays a pivotal role in regulating various physiological processes in the body such as metabolism, secretion and storage. ROS modify or damage biomolecules, i.e., proteins, lipids, carbohydrates and DNA [3]. Oxidative stress lead to the formation of glycoxidation products, including advanced glycation end products (AGEs - among them Nε-(carboxymethyl) lysine (CML) is best known), and advanced oxidation protein products (AOPPs). The receptor for advanced glycation end products (RAGE) is a signal transduction receptor that binds both AGEs and AOPPs. RAGE is expressed by hepatic stellate cells and myofibroblasts, which are the relevant cells for fibrogenesis of chronic liver disease. RAGE is expressed by hepatic stellate cells and myofibroblasts, which are the relevant cells for fibrogenesis of chronic liver disease Both AGEs and AOPPs trigger the inflammatory response via interaction with RAGE and by causing activation of nuclear factor NF-B [4]. Since advanced oxidation protein products are markers of oxidative stress and act as inflammatory mediators [5], the knowledge of AOPPs pathophysiology in chronic liver disease could provide valuable information with respect to the relationship between oxidative stress and the inflammatory response related to liver fibrosis [6]

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