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The purpose of this study was to analyze the role of gallic acid as liver protector and identify its role in the regulation of EGFR expression and phosphorylation in induced preneoplastic liver lesions in rats. Male Wistar rats were randomly divided into four groups. (1) Control; (2) animals receiving gallic acid (AG) 50 mg/kg v.o. for 8 weeks; (3) animals with preneoplasia (P) induced by a single dose of diethylnitrosamine 200 mg/kg i.p. (DEN) and two weeks after a single dose of carbon tetrachloride 2 mL/kg i.p. (CCl4); and (4) animals with preneoplasia treated with GA during 8 weeks. In order to evaluate GA hepatoprotection on preneoplastic lesions, we performed histological examination of liver tissue using H&E staining as well as an immunohistochemical analysis for PCNA. To evaluate the effect of GA on EGFR expression and phosphorylation, we performed an immunohistochemical and western blot analysis. The results indicated that GA significantly decreased EGFR expression and pY1068 EGFR phosphorylation in animals with preneoplastic lesions. GA significantly decreased PCNA expression in animals with preneoplastic lesions, suggesting it may work as an antiproliferative agent. Additionally, GA improved the architecture and organization of liver tissue and significantly decreased serum AST, ALT and FA, which are indicators of hepatocellular damage. By histopathological and immunohistochemical analysis we demonstrated an improvement in liver morphology, a reduction of preneoplastic liver foci and a reduction of cell proliferation, as well as an improvement on liver functionality. In conclusion, GA produces hepatoprotection by modulating EGFR expression and phosphorylation in preneoplastic lesions.

Gallic acid produces hepatoprotection by modulating EGFR expression and phosphorylation in induced preneoplastic liver foci in rats