D-Pinitol prevents rat breast carcinogenesis induced by 7, 12 -Dimethylbenz [a] anthracene through inhibition of Bcl-2 and induction of p53, caspase-3 proteins and modulation of hepatic biotransformation enzymes and antioxidants

Abstract

Dietary compounds are reported to have the innate ability to interfere several diseases. D-Pinitol is one of the compounds from dietary origin, well documented for its excellent biological activities. We have reported the therapeutic efficiency of the D-Pinitol with reference to lipid peroxidation, antioxidants, drug metabolizing enzymes and expressions of proteins such as p53, Bcl-2, and caspase-3 during DMBA-induced mammary carcinogenesis. D-Pinitol at the dose of 200mg/kg body weight was administered orally to treat the breast cancer-bearing animals for consecutive 45 days. Interestingly, D-Pinitol significantly decreased the lipid peroxidation and increased the antioxidants and modulated the biotransformation enzymes to near normal level when compared to control. The western blotting and RT-PCR analysis also inevitably confirms that D-Pinitol treatment down regulated the expression of Bcl-2 and up regulated the p53 and caspase-3 proteins. The histological analysis of breast and liver tissues were well supported the protective role of D-Pinitol. Thus, the therapeutic property of D-Pinitol might be due to its strong antioxidant and remarkable induction in phase II and significant modulation in phase I drug metabolizing enzymes and prominent influence in the proteins of apoptotic, anti-apoptotic and tumor suppressors which ultimately end up with the consideration of D-Pinitol in the treatment of genotoxin mediated carcinogenesis.