The change of transforming growth factor-beta1 expression and the effect of vitamin E in the acute rat liver injury with carbon tetrachloride

Abstract

Background/ A ims : The evaluation of the relationship between oxidative stress induced by acute carbon tetrachloride (CCl4 ) administration and transforming growth factor -β1 (T GF -β1), and the investigation of temporal patterns of serum alanine aminotransferase (ALT ) and T GF-β1 expression which may clarify the pathogenesis of CCl4 induced liver injury and thus the mechanism of liver fibrogenesis. The aim of this study was to investigate T GF -β1 expression in rats with acute CCl4 injury and effect of vitamin E (vit . E) on T GF-β1 expression. Methods : Sixty male Sprague-Dawley rats had a single intraperitoneal injection of CCl4 , of which 30 rats had daily intraperitoneal injection of vit . E, starting from 2 days before CCl4 treatment until the time of their sacrifice. The group of rats with CCl4 injection only was designated as group 1 and the group of rats with vit . E combined treatment was designated as group 2. Five rats from each group were sacrificed before and 8, 16, 32, 48, 60 hours after CCl4 injection, and their serum ALT , serum T GF -β1, and hepatic expression of T GF-β1 were examined. Result s : The serum ALT levels were highest at 32 hours after CCl4 injection in both groups, serum T GF -β1 levels did not show any statistically significant changes after CCl4 injection in both groups, and T GF -β1 expression in the livers was highest at 32 hours after CCl4 injection in both groups. In the multiple regression analysis of vit . E ' s effect on serum ALT levels, serum T GF-β1 levels and hepatic T GF-β1 expression, only serum ALT level (p=0.049) and hepatic T GF-β1 expression (p=0.015) showed statistically significant suppression. Conclusion : Oxidative stress seems to play a role in the pathogenesis of hepatic fibrogenesis by increasing T GF -β1 expression in early acute liver damage. and vit . E may be effective in reducing acute liver injury and hepatic fibrogenesis. (Korean J Hepatol 2000;6:147155)