Fermented papaya preparation halts the progression of non-alcoholic steatohepatitis in rats

Shinki Murakami,Mitsuko Imao,Fusako Takayama,Toru Egashira,Akitane Mori

doi:10.4236/jbpc.2013.42012

Abstract

Non-alcoholic steatohepatitis (NASH) can progress to cirrhosis or hepatocellular carcinoma. Oxidative stress is implicated in NASH progression. Fermented papaya preparation (FPP) has oxygen radical scavenging activity and is effective in oxidative stress-related diseases. We investigated the effects of FPP on NASH progression using a rat NASH model. Plasma biochemical parameters and lipid peroxidation in the liver were elevated in NASH rats. Histologically, the liver of NASH rats showed liver fibrosis, mitochondrial dysfunction and over-expression of microsomal CYP2E1. Myeloperoxidase activity and nuclear factor-kappaB activation were also markedly increased in NASH. Oral administration of FPP ameliorated these changes in NASH rats. These results suggest that FPP halts NASH progression through its anti-oxidative and antiinflammatory properties.

Highlights

Non-alcoholic fatty liver disease (NAFLD) is the most frequent cause of liver damage, closely associated with obesity and the metabolic syndrome, and often progresses to non-alcoholic steatohepatitis (NASH)
Macrovesicular hepatic steatoses were evident in the liver of choline-deficient high-fat (CDHF)-treated rats, and marked fibril formations were observed in the liver of NASH rats by Masson-trichrome staining
The present study demonstrated the preventive effects of oral Fermented papaya preparation (FPP) administration on NASH progression

Summary

Introduction

Non-alcoholic fatty liver disease (NAFLD) is the most frequent cause of liver damage, closely associated with obesity and the metabolic syndrome, and often progresses to non-alcoholic steatohepatitis (NASH). We previously established a clinically relevant rat model of NASH (Patent application No PCT/JP2007/52477) [3] This model is prepared as follows; rats are fed a choline-deficient high-fat diet for 4 weeks to induce steatosis, and are treated by intraperitoneal injections of nitrite for 6 weeks to induce hypoxia-related oxidative stress. Using this model, it has been demonstrated that OS causes extensive hepatic fibrosis, and that these effects can be ameliorated by anti-oxidants, such as fermented green tea extract [4], vitis coignetiae pulliat leaves [5,6], docosahexaenoic acid [7], and spirulina [8]

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Conclusion