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Quercetin Reverses Rat Liver Preneoplastic Lesions Induced by Chemical Carcinogenesis

Quercetin is a flavonoid widely studied as a chemopreventive agent in different types of cancer. Previously, we reported that quercetin has a chemopreventive effect on the liver-induced preneoplastic lesions in rats. Here, we evaluated if quercetin was able not only to prevent but also to reverse ra...

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Detalles Bibliográficos
Autores principales: Carrasco-Torres, Gabriela, Monroy-Ramírez, Hugo Christian, Martínez-Guerra, Arturo Axayacatl, Baltiérrez-Hoyos, Rafael, Romero-Tlalolini, María de los Ángeles, Villa-Treviño, Saúl, Sánchez-Chino, Xariss, Vásquez-Garzón, Verónica Rocío
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504959/
https://www.ncbi.nlm.nih.gov/pubmed/28740570
http://dx.doi.org/10.1155/2017/4674918
Descripción
Sumario:Quercetin is a flavonoid widely studied as a chemopreventive agent in different types of cancer. Previously, we reported that quercetin has a chemopreventive effect on the liver-induced preneoplastic lesions in rats. Here, we evaluated if quercetin was able not only to prevent but also to reverse rat liver preneoplastic lesions. We used the modified resistant hepatocyte model (MRHM) to evaluate this possibility. Treatment with quercetin was used 15 days after the induction of preneoplastic lesions. We found that quercetin reverses the number of preneoplastic lesions and their areas. Our results showed that quercetin downregulates the expression of EGFR and modulates this signaling pathway in spite of the activated status of EGFR as detected by the upregulation of this receptor, with respect to that observed in control rats. Besides, quercetin affects the phosphorylation status of Src-1, STAT5, and Sp-1. The better status of the liver after the treatment with quercetin could also be confirmed by the recovery in the expression of IGF-1. In conclusion, we suggest that quercetin reversed preneoplastic lesions by EGFR modulation and the activation state of Src, STAT5, and Sp1, so as the basal IGF-1.