Modulatory Influence of Dietary Gallic Acid on Molecular Markers in 1, 2 Dimethylhydrazine–induced Colon Carcinogenesis in an Experimental Rat Model

Our aim was to explore the modulatory effect of gallic acid (GA) preneoplastic and neoplastic markers employing 1,2-dimethylhydrazine (DMH) induced colon cancer in male Wistar rats as an experimental model during the different stages of carcinogenesis. Group 1 served as control, group 2 rats were given GA, 50mg/kg body weight by intragastric intubation everyday; groups 3-6 were injected DMH (s.c. injections, 20mg/kg body weight) once a week for the first 15 weeks. Group 4 rats received GA as in group 2 starting 1 week before DMH injections and continued till the final exposure [DMH + GA (I)]. Group 5 rats received GA as in group 2 after the cessation of DMH injections and continued till the end [DMH + GA (PI)] of the experimental period. The rats in group 6 were supplemented with GA as in group 2 from the day of carcinogen treatment and continued till the end of the entire experimental period of 32 weeks *DMH+GA (EP)+. Colon tissues were analyzed for the expression of βcatenin, proliferating cell nuclear antigen (PCNA) and argyrophilic nucleolar organizer regions (AgNORs) by using immunohistochemistry and silver staining. Immunoblotting was employed to study cyclin D1 expression and preneoplastic changes. GA inhibited DMH-induced colon cancer by decreasing tumour incidence, multiplicity and also the formation ACF. Supplementation with GA to DMH-treated rats decreased the levels of β-catenin, PCNA, AgNORs and cyclin D1. Since colon cancer is highly sensitive to dietary intervention, adults who may have preneoplastic lesions in their colon may be benefited by GA.