Abstract

BackgroundActivin-A and follistatin regulate the liver and the immune system.AimsTo measure the effects of treatment with pegylated-interferon-α (Peg-IFN-α) and ribavirin on the concentrations of mature activin-A and follistatin in serum and liver tissue homogenates in rats.MethodsA total of 28 male Wistar rats were divided equally into four groups as follow: ‘Control group’ (n = 7), ‘PEG only group’ consisted of those that only received a weekly injection of Peg-IFN-α (6 µg/rat) for 4 weeks, ‘RBV only group’ received ribavirin only (4 mg/rat/day) orally for 35 days and the last group received both Peg-IFN-α and ribavirin ‘PEG & RBV group’. The concentrations of candidate proteins in serum and liver samples were measured using ELISA.ResultsPegylated-interferon-α decreased activin-A and increased follistatin significantly in serum and liver of ‘PEG only’ and ‘PEG & RBV’ groups compared with the ‘Control’ and ‘RBV only’ groups (P < 0.05). There was no significant difference between the ‘RBV only’ and ‘Control’ groups (P > 0.05) in the concentrations of candidate proteins. A significant positive correlations between serum and liver activin-A (r = 0.727; P = 0.02 × 10−3) and follistatin (r = 0.540; P = 0.01) was also detected.ConclusionPegylated-interferon-α modulates the production of activin-A and follistatin by the liver, which is reflected and can be detected at the serum level. Further studies are needed to explore the role of Peg-IFN-α based therapy on the production of activins and follistatin by the liver and immune cells.

Highlights

  • Activin-A and follistatin regulate the liver and the immune system

  • Pegylated-interferon-α modulates the production of activin-A and follistatin by the liver, which is reflected and can be detected at the serum level

  • Further studies are needed to explore the role of Peg-IFN-α based therapy on the production of activins and follistatin by the liver and immune cells

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Summary

Introduction

Infection with hepatitis C virus (HCV) is a global health problem and it is a leading cause for the development of liver fibrosis, cirrhosis and hepatocellular carcinoma [1]. The development of hepatic complications following infection with HCV is due the promotion of adaptive immune response by activating T helper (Th)-2 pathway [8, 9]. Activin-A and follistatin are expressed by the hepatocyte and have been described as major regulators of liver biology, liver regeneration and liver pathology [16]. They play an important role in the regulation of the immune system and the pathogenesis of inflammatory and fibrotic human diseases [17]

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