Genistein Produces Hepatoprotection through Modulating EGFR Expression and Phosphorylation in Experimental Fibrosis

Abstract

Background and Objective: Liver disease chronicity leads to the appearance of fibrosis, cirrhosis, and eventually cancer. For this reason, it is important to research new fibrosis therapies. The use of genistein as a hepatoprotective agent has been studied, but its mechanism of action is unknown. The aim of this work was to evaluate the role of genistein as a fibrosis treatment and its possible mechanism of action through CCl4-induced inhibition of EGFR in rat specimens. Methods: Hepatic fibrosis was brought about by chronic administration of CCl4 to rats. Animals with fibrosis were treated with 1 mg/kg genistein. To evaluate the hepatoprotection of genistein on liver fibrosis, we made a histopathological analysis using both HE PCNA positive cells were reduced in this group. We observed liver functionality improvement in those animals with fibrosis that were treated with genistein. Conclusion: Genistein produces hepatoprotection through modulating the expression and phosphorylation of EGFR in experimental fibrosis.