β-Alanyl-L-Histidine, an Anti-Oxidant, Anti-fibrotic and Geno/Cytotoxicity Inhibitor: A Sheild against CCl4-Induced Hepatotoxicity in Rats

Abstract

Hepatic fibrosis is a consequence of chronic liver injury and is characterized by an excessive hepatic connective tissue formation and deposition. β-alanyl-L-histidine (carnosine) is a dipeptide with antiinflammatory 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 β-alanyl-L-histidine against hepatic injury induced by carbon tetrachloride (CCl₄) in rats. β-alanyl-Lhistidine showed significant protection with normalization of liver aminotransferases, increased glutathione S transferase (GST) activity while decreased hepatic hydroxyproline, protein carbonyl, hydrogen peroxide (H₂O₂) levels, DNA damage, Cytochrome P450₂E₁ (CYP₂E₁) activity and transforming growth factor-β1 (TGF-β1) mRNA level. In conclusion: β-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.

Key words: β-alanyl-L-histidine; Carbon tetrachloride; Cytochrome P4502E1; Transforming growth factor -β1