RESUMEN
Hepatic fibrosis is a consequence of chronic liver injury and is characterized by an excessive hepatic connective tissue formation and deposition. p-alanyl-L-histidine [carnosine] is a dipeptide with anti-inflammatory and antioxidant properties in addition to its involvement in many physiological process. Specific treatments to stop progressive liver fibrosis are not available, so that the objective of the present study was to evaluate the hepatoprotective, antioxidant, antifibrotic, cyto/genoprotective effect of p-alanyl-L-histidine against hepatic injury induced by carbon tetrachloride [CCU] in rats. p-alanyl-L-histidine showed significant protection with normalization of liver aminotransferases, increased glutathione S transferase [GST] activity while decreased hepatic hydroxyproline, protein carbonyl, hydrogen peroxide[H[2]O[2]] levels, DNA damage, Cytochrome P450[2]Ei [CYP[2]Ei] activity and transforming growth factor-pi [TGF-pl] mRNA level. In conclusion: P-alanyl-L-histidine possesses hepatoprotective properties through reducing hepatic toxicity markers, oxidative stress, cytotoxicity, genotoxicity, fibrosis and improvement of the histological architecture of the liver