Hepatoprotective Effect of Carvacrol on Carbon Tetrachloride Induced Liver Toxicity in Adult Albino Rats, MOSTAFA M. ABD EL-MONEM, MONA A. EL-SHAHAT, HUSSEIN M.H. ABD EL-LATIF and OLA M. YOUSSEF ALI
Abstract
Background: Liver fibrosis is a major health problem associated with high morbidity and mortality, particularly in Egypt. It is mainly regulated by hepatic stellate cells, which acquire a fibrogenic character in response to oxidant stress and inflammatory cytokines.
Aim of Study: This study was designed to evaluate the possible hepatoprotective effect of carvacrol on carbon tetra-chloride (CCL4) treated rats as a model for liver fibrosis.
Material and Method: Twenty four adult female albino rats were divided into 3 groups, the 1st group served as control group, the 2nd group (CCL4 treated group) served as model of fibrosis, the 3rd group received CCL4 plus carvacrol and the 4th group served as a sham control group received corn oil. Serum Alanine Transaminase (ALT) and Aspartate Transaminase (AST) were estimated for assessment of liver functions. Reduced Glutathione (GSH) and Malonaldehyde (MDA) in liver tissues were evaluated. The liver samples were prepared and stained with haematoxylin and eosin (H & E) and Picro-Sirius red.
Results: It was found that there was no significant differ-ence between control and sham groups. In the CCL4 treated group, there was increase in the level of liver enzymes. MDA was increased and GSH was decreased. Histopathological examination showed loss in liver architecture with marked degeneration of hepatocytes. On evaluation of distribution of fibrous tissue by Sirius red stain, fibrous tissue septa were distributed all over the sections. In the carvacrol treated group simultaneously with CCL4, both biochemical and histopatho-logical results were significantly better than the results of CCL4 treated group.
Conclusion: The present study illustrates that CCL4 caused liver toxicity, histological alterations, fibrosis and disturbed liver function. Carvacrol possesses a hepatoprotective effect against CCL4 induced liver toxicity and fibrosis proved by the significant decrease in serum ALT and AST and significant decrease in the fibrosis area and preservation of liver archi-tecture. This may be through its antioxidant effect, proved by the decrease in liver MDA and the increase in liver GSH.