Abstract
In this study we investigated if ghrelin plays a protective role against paracetamol-induced acute hepatotoxicity in rats and the possible mechanism of action. Forty adult male albino rats were divided into four equal groups; control, ghrelin, paracetamol and ghrelin plus paracetamol. Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Liver histopathology was also performed. Paracetamol (PCM) treatment increased plasma and liver tissue malondialdehyde (MDA) content and plasma nitric oxide (NO) level, and decreased erythrocyte and liver tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities when compared to control group. At the same time, PCM treatment increased the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities. By contrast, ghrelin pretreatment reduced plasma and liver MDA content and plasma NO level, and increased erythrocyte, liver tissue SOD, CAT and GPx activities when compared with paracetamol-treated group. The PCM-induced histopathological changes were also reduced by the ghrelin pretreatment. In conclusion, our results proved that ghrelin was found to protect the liver against paracetamol-induced oxidative damage in rats and the hepatoprotective effect may be correlated with its antioxidant effect. Key words: Antioxidant, ghrelin, hepatoprotective, hepatotoxicity, paracetamol.
Highlights
INTRODUCTIONA 28 amino acid peptide, was recognized as the main endogenous ligand for the growth hormone secretagogue receptor (GHSR) (Kojima et al, 1999)
Ghrelin, a 28 amino acid peptide, was recognized as the main endogenous ligand for the growth hormone secretagogue receptor (GHSR) (Kojima et al, 1999).Ghrelin is secreted primarily from the stomach, but ghrelin transcripts have been found in many other organs, including the liver, kidney, lung, pancreas, hypothalamus and heart, suggesting an endocrine as well as extra-endocrine action of ghrelin (Kojima et al, 1999; Gnanapavan et al, 2002)
Our findings demonstrated that ghrelin exerts a potent protective effect against PCMinduced acute liver injury by increasing superoxide dismutase (SOD), CAT and
Summary
A 28 amino acid peptide, was recognized as the main endogenous ligand for the growth hormone secretagogue receptor (GHSR) (Kojima et al, 1999). Kheradmand et al (2010) reported that ghrelin promotes antioxidant enzyme activity and reduces lipid peroxidation in the rat ovary. (2008) have shown that ghrelin prevents lipid peroxidation and reduction of antioxidant enzyme activities and glutathione level against pentylenetetrazole-induced oxidative stress in the erythrocytes, liver and brain of rats. Xu et al (2008) demonstrated that ghrelin significantly reduced the concentration of malondialdehyde and increased the activity of antioxidant enzymes such as superoxide dismutase and catalase in primary cultured cardiomyocytes. Oxidative stress was reported to play a fundamental role in the pathogenesis of PCM-induced liver damage (Srinivasan et al, 2001). The present study aims to investigate the possible protective effect of ghrelin on PCM induced hepatotoxicity by studying its effect on serum liver functions and oxidative stress biomarkers, as well as on hepatic histopathology of the rat
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