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Abstract
The aim of the present study was to investigate the potential antioxidant and Hepatoprotective activities of tranilast against TAA-induced liver fibrosis in rats. Methods: Liver fibrosis was induced in rats by intra peritoneal injection of TAA (200 mg/kg) for 6 weeks. Tranilast was administered orally at a dose of 150 and 300mg/kg for 6 weeks before induction of liver fibrosis. Results: Injection of TAA induced hepatic fibrosis that was manifested by a significant increase in the activities of aminotransferases and total bilirubin with a significant decrease in total protein and albumin in serum. Liver homogenate of TAA rats had the lower content of reduced glutathione (GSH) and superoxide dismutase (SOD) with increased levels of the hepatic malondialdehyde. Histological data presented marked damage in liver sections of TAA rats. Oral dosing of tranilast for 6 weeks before induction of liver fibrosis reversed these altered parameters near to normal values. These results suggest that tranilast could afford significant protection and antioxidant effect in prevention of liver fibrosis.
Highlights
Liver fibrosis is defined as the hepatic dynamic response to repeated and chronic liver injury, accompanying the activation of HSCs, the over expression of extracellular matrix (ECM) proteins, lead to cirrhosis, which is characterized by scar tissue, loss of parenchymal architecture and organ failure (Wang et al 2016)
The data in table (1) revealed that, after 6 weeks of TAA injection, there was a significant elevation of serum levels of hepatic enzymes (ALT and AST) and total bilirubin with a significant reduction of total protein and albumin levels compared to normal control
The results showed that GSH content and superoxide dismutase (SOD) activity were significantly reduced and MDA level was significantly increased in TAA induced liver fibrosis rats, compared to normal control
Summary
Liver fibrosis is defined as the hepatic dynamic response to repeated and chronic liver injury, accompanying the activation of HSCs, the over expression of extracellular matrix (ECM) proteins, lead to cirrhosis, which is characterized by scar tissue, loss of parenchymal architecture and organ failure (Wang et al 2016). TAA is a model hepatotoxicant and responsible of severe damage of the cells with significant toxic effects on the biosynthesis of macromolecules including proteins and nucleic acid. Different studies showed that the exposure to TAA caused liver injury, fibrosis and cirrhosis in experimental animals. The hepatic toxic chemical TAA has been widely used in the study of the underlying mechanisms of hepatic fibrogenesis and the therapeutic effects of potential antifibrotic drugs (Al-Attar et al 2016)
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