Journal
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
Volume 72, Issue 7, Pages 1657-1666Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1271/bbb.70473
Keywords
D-galactosamine; hepatotoxicity; tumor necrosis factor-alpha (TNF-alpha); pinitol; rat
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The protective effect of pinitol against D-galactosamine (GalN)-induced liver damage was examined. Forty male Sprague-Dawley rats were divided into normal control, GaIN control, and pinitol groups (0.5%, 1 %, and 2%). After 8 weeks of feeding, a single dose of GaIN (650 mg/kg) was administered 24h before their sacrifice. The serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor-alpha TNF-alpha levels were significantly increased after an injection with GaIN (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 GaIN, at least part of its effect being attributable to attenuation of the oxidative stress and inflammatory process promoted by GaIN.
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