alexa Genistein Produces Hepatoprotection through Modulating EGFR Expression and Phosphorylation in Experimental Fibrosis
ISSN: 2167-0889

Journal of Liver
Open Access

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Research Article

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

Rodriguez Fragoso L1*, Alvarez Ayala E1, García Vazquez F2 and Reyes Esparza J1

1Universidad Autónoma del Estado de Morelos, Cuernavaca, Mexico

2Department of Science, Pathology, National Institute of Pediatrics, Cuernavaca, Mexico

*Corresponding Author:
Fragoso LR
Faculty of Pharmacy
Universidad Autónoma del Estado de Morelos
Cuernavaca, Mexico
Tel: 052 5 777329 7089
E-mail: [email protected]

Received date: April 23, 2016; Accepted date: June 07, 2016; Published date: June 15, 2016

Citation: Fragoso RL, Ayala AE, Vazquez GF, Esparza JR (2016) Genistein Produces Hepatoprotection through Modulating EGFR Expression and Phosphorylation in Experimental Fibrosis. J Liver 5:196. doi:10.4172/2167-0889.1000196

Copyright: © 2016 Fragoso LR et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

 

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 H&E and trichrome staining, as well as an immunofluorescence analysis for α- SMA and an immunohistochemical analysis for PCNA. In order to find out the effects of genistein on EGFR expression and phosphorylation, we performed immunostaining for EGFR and dot blot analysis for two specific tyrosine residues: pY992 and pY1068. We also evaluated liver functionality. Results: Genistein reduced liver fibrosis and improved liver architecture. α-SMA positive cells were lower in genistein-treated animals with fibrosis. Likewise we found a reduction in EGFR expression and phosphorylation of genistein-treated animals with fibrosis; 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.

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