Protective Effect of Pinitol against <small>D</small>-Galactosamine-Induced Hepatotoxicity in Rats Fed on a High-Fat Diet

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  • ZHOU Yusi
    Department of Food and Nutrition, Food Science Institute and BPRC, Inje University
  • PARK Chung-Mu
    Department of Food and Nutrition, Food Science Institute and BPRC, Inje University
  • CHO Chung-Won
    School of Biotechnology and Biomedical Science, Inje University
  • SONG Young-Sun
    Department of Food and Nutrition, Food Science Institute and BPRC, Inje University

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  • Protective effect of pinitol against D-galactosamine-induced hepatotoxicity in rats fed on a high-fat diet
  • Protective Effect of Pinitol against<scp>D</scp>-Galactosamine-Induced Hepatotoxicity in Rats Fed on a High-Fat Diet

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Abstract

The protective effect of pinitol against D-galactosamine (GalN)-induced liver damage was examined. Forty male Sprague-Dawley rats were divided into normal control, GalN control, and pinitol groups (0.5%, 1%, and 2%). After 8 weeks of feeding, a single dose of GalN (650 mg/kg) was administered 24 h before their sacrifice. The serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor-alpha (TNF-α) levels were significantly increased after an injection with GalN (P<0.05), but pinitol supplementation at the level of 0.5% reversed these changes to normal levels. Significant decreases in serum triglyceride and cholesterol and increases in hepatic cholesterol were observed in GalN-intoxicated rats. However, supplementation with pinitol significantly attenuated these trends. In addition, pinitol elevated the Mn-superoxide dismutase, glutathione reductase, and catalase activities, prevented hepatic lipid peroxidation, and restored the hepatic GSH levels and cytochrome P450 2E1 function. Thus, 0.5% pinitol supplementation protected the rats from the hepatotoxicity induced by GalN, at least part of its effect being attributable to attenuation of the oxidative stress and inflammatory process promoted by GalN.

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