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Title of Journal: Mol Cell Biochem

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Abbravation: Molecular and Cellular Biochemistry

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Springer US

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DOI

10.1002/cncr.20872

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1573-4919

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Glycyrrhizin ameliorates metabolic syndromeinduce

Authors: Rajarshi Sil Doel Ray Abhay Sankar Chakraborti
Publish Date: 2015/09/23
Volume: 409, Issue: 1-2, Pages: 177-189
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Abstract

Glycyrrhizin a major constituent of licorice Glycyrrhiza glabra root has been reported to ameliorate insulin resistance hyperglycemia dyslipidemia and obesity in rats with metabolic syndrome Liver dysfunction is associated with this syndrome The objective of this study is to investigate the effect of glycyrrhizin treatment on metabolic syndromeinduced liver damage After induction of metabolic syndrome in rats by high fructose 60  diet for 6 weeks the rats were treated with glycyrrhizin 50 mg/kg body weight single intraperitoneal injection After 2 weeks of treatment rats were sacrificed to collect blood samples and liver tissues Compared to normal elevated activities of serum alanine transaminase alkaline phosphatase and aspartate transaminase increased levels of liver advanced glycation end products reactive oxygen species lipid peroxidation protein carbonyl protein kinase Cα NADPH oxidase2 and decreased glutathione cycle components established liver damage and oxidative stress in fructosefed rats Activation of nuclear factor κB mitogenactivated protein kinase pathways as well as signals from mitochondria were found to be involved in liver cell apoptosis Increased levels of cyclooxygenase2 tumor necrosis factor and interleukin12 proteins suggested hepatic inflammation Metabolic syndrome caused hepatic DNA damage and polyADP ribose polymerase cleavage Fluorescenceactivated cell sorting using annexin V/propidium iodide staining confirmed the apoptotic hepatic cell death Histology of liver tissue also supported the experimental findings Treatment with glycyrrhizin reduced oxidative stress hepatic inflammation and apoptotic cell death in fructosefed rats The results suggest that glycyrrhizin possesses therapeutic potential against hepatocellular damage in metabolic syndromeR S received research fellowship from University Grants Commission UGC India D R received research fellowship from Council of Scientific and Industrial Research CSIR India Assistances from the Departmental Special Assistance Programme of UGC and Centre for Research in Nanoscience and Nanotechnology CRNN University of Calcutta are gratefully acknowledged


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