The protective and chemotherapeutical role of amygdalin in induced mammary cancer in experimental mice and upregulation of related genes.

Breast cancer is a prominent health issue among oncological diseases in emerging nations. The study sought to assess the significant function of amygdalin as a protective and chemotherapeutical substance in combating this lethal condition, either independently or in conjunction with tamoxifen therapy. Breast cancer in mice was induced by 7,12-Dimethylbenz(a)anthracene (DMBA). Mice were divided into six groups, 15 mice in each group. (i) control group, (ii) carcinogenic group, (iii) tamoxifen-treated group, (iv) Amygdalin-treated group, (v) (Amygdalin + tamoxifen) group, (vi) Amygdalin protective group. Results revealed that DMBA-induced breast cancer caused a significant increase in biochemical parameters such as CEA, CA15.3, CA125, PRL, E2, urea, creatinine, ALT, AST, and ALP and a substantial increase in gene expression of TNF-α and BcL-2. In contrast, amygdalin administrations alone or in co-administration with tamoxifen could ameliorate breast cancer by declining TNF-α, BcL-2 and attenuating the biochemical parameters. Amygdalin administrations showed a significant increase in SOD and GPx antioxidants and upregulation of Caspase-3 and P53 in breast tissue. Moreover, flow cytometric analysis revealed that amygdalin administrations were correlated with CD20 and CD44 and promoted the cell cycle and apoptosis in carcinogenic mice. Indeed, the above results were confirmed by the histopathological examinations, which showed that the DMBA group had proliferated microductular carcinoma with marked mononuclear inflammatory cell infiltration, which decreased by the Amygdalin administrations. In conclusion, amygdalin administration may be effective in preventing breast cancer and exhibiting chemotherapeutic properties.