Abstract

The aim of this study was to investigate the chemical constituents of petroleum ether extract from Artemisia integrifolia L (AIPEE) and to evaluate its hepatoprotective potential and in vivo antioxidant effects. Six compounds, namely eugenol (1), linolenic acid (2), 6,7-epoxy-linolenic acid (3), linoleic acid (4), oleic acid (5) and hexadecanoic acid (6) were isolated from the AIPEE. Oral administration of AIPEE significantly reduced carbon tetrachloride-induced elevations in the levels of plasma markers of hepatic damage and lipid peroxidation. It also rescued histopathologic alterations observed in the liver and levels of oxidative stress markers. AIPEE exhibited antioxidant and hepatoprotective activities in vivo, which may be attributable to its chemical constituents such as five fatty acids and eugenol. Key words: Artemisia integrifolia L., fatty acids, eugenol, antioxidant, hepatoprotection.

Highlights

  • Liver is the most important organ, which is involved in several vital functions, for example, metabolism, secretion and storage (Sharma et al, 2012; Mistry et al, 2013)

  • The aim of this study was to investigate the chemical constituents of petroleum ether extract from Artemisia integrifolia L (AIPEE) and to evaluate its hepatoprotective potential and in vivo antioxidant effects

  • AIPEE was separated by chromatography and assigned six compounds, namely eugenol (1), linolenic acid (2), 6,7-epoxy-linolenic acid (3), linoleic acid (4), oleic acid (5) and hexadecanoic acid (6) (Figure 2)

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Summary

Introduction

Liver is the most important organ, which is involved in several vital functions, for example, metabolism, secretion and storage (Sharma et al, 2012; Mistry et al, 2013). An important factor that induces liver fibrosis, represents a key feature of hepatitis induced by various conditions, including anoxic/reoxygenation injury, autoimmune hepatitis, viral hepatitis, and alcoholic hepatitis (Singh et al, 2008). The CCl4-induced liver toxicity model is widely used because CCl4 induces hepatic changes analogous to those observed in chemical hepatitis. CCl4 is converted by the cytochrome P450 system into a trichloromethyl radical. This radical reacts with oxygen to form a trichloromethylperoxyl radical, which reacts with cell macromolecules, inducing lipid peroxidation and provoking hepatocyte membrane breakdown (Halliwell, 2012)

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