Abstract

In oriental medicine, curcumin is used to treat inflammatory diseases, and its anti-inflammatory effect has been reported in recent research. In this feasibility study, the hepatoprotective effect of curcumin was investigated using a rat liver cirrhosis model, which was induced with dimethylnitrosamine (DMN). Together with biochemical analysis, we used a magnetic resonance-based electrical conductivity imaging method to evaluate tissue conditions associated with a protective effect. The effects of curcumin treatment and lactulose treatment on liver cirrhosis were compared. Electrical conductivity images indicated that liver tissues damaged by DMN showed decreased conductivity compared with normal liver tissues. In contrast, cirrhotic liver tissues treated with curcumin or lactulose showed increased conductivity than tissues in the DMN-only group. Specifically, conductivity of cirrhotic liver after curcumin treatment was similar to that of normal liver tissues. Histological staining and immunohistochemical examination showed significant levels of attenuated fibrosis and decreased inflammatory response after both curcumin and lactulose treatments compared with damaged liver tissues by DMN. The conductivity imaging and biochemical examination results indicate that curcumin's anti-inflammatory effect can prevent the progression of irreversible liver dysfunction.

Highlights

  • Cirrhosis is histologically defined as an advanced fibrosis of liver tissues

  • Comparison of normal and DMN-only groups showed that the aspartate transaminase (AST) and alanine transaminase (ALT) levels in the DMN-only group were significantly higher than those in the normal control group, indicating the progression of liver injury

  • Comparison of treatment groups and the DMN-only group showed that the DMN with curcumin group exhibited significantly lower AST and ALT values than the DMN-only group, whereas the DMN with lactulose group exhibited significantly lower values only for ALT

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Summary

Introduction

Cirrhosis is histologically defined as an advanced fibrosis of liver tissues. Liver fibrosis is a hepatic response to chronic injury and is characterized by excess deposition of collagen, proteoglycans, and other macromolecules in the extracellular matrix [1]. These result in tissue degeneration and lead to portal hypertension and end-stage liver disease [1]. Histological changes from cirrhosis were considered irreversible, but recent studies have reported that liver fibrosis, even the more advanced stages, can be ameliorated with appropriate therapy [2]. The appropriate therapy may help to extend the life span of patients with liver fibrosis from a long-term perspective

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