The therapeutic effects of tectorigenin on chemically induced liver fibrosis in rats and an associated metabonomic investigation.

The aim of this study was to investigate the effects of tectorigenin on chemically induced liver fibrosis in rats. Liver fibrosis was induced in rats with carbon tetrachloride, a diet high in fat, cholesterol and alcohol in the drinking water. Our results indicate that tectorigenin treatment significantly inhibited the increases in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and the increases in the serum levels of hyaluronate (HA), laminin (LN) and procollagen III N-terminal peptide (PIIIP); tectorigenin treatment also significantly inhibited the increases in the amount of collagen in the livers of the fibrogenic rats. Chemically induced liver fibrosis caused a drop in the serum albumin concentration and a decrease in the ratio of albumin to globulin (A/G). Tectorigenin caused a remarkable increase at a dose of 30 mg/kg, but only a slight increase at the lower doses. Tectorigenin was also able to inhibit the increase in the liver lipid peroxidation (LPO), as well as the decrease in the activities of liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), caused by liver fibrosis. In addition, we present a related metabolic profile determined, using a (1)H NMR spectroscopy and multivariate pattern recognition techniques. The results were consistent with the pathological examination, liver function analysis and liver fibrosis marker analysis. Furthermore, tectorigenin does not cause acute toxicity.