BACKGROUND/AIM: The expression of cannabinoid receptor-1 (CB1-R) seems to be modulated by bioactive natural components such as the flavonoid quercetin. The aim of this study was to determine in an animal model of induced-colon cancer, whether quercetin inhibits colon carcinogenesis through changes in the expression of CB1-R.
MATERIALS AND METHODS: C57BL/6J male mice were randomly assigned to standard diet or experimental diet supplemented with 0.5% quercetin. Azoxymethane (AOM) (10 mg/kg body weight) or saline solution (PBS) was intraperitoneally injected, once weekly for 6 weeks.
RESULTS: The diet supplemented with quercetin induced CB1-R gene expression and protein, inhibiting the protein levels of STAT3 and p-STAT3 (both mediators of cell proliferation). Dietary quercetin also caused a significant increase in Bax/Bcl2 ratio protein expression.
CONCLUSION: The anti-proliferative and pro-apoptotic effects of quercetin in AOM-treated mice are mediated by induction of the protein and gene expression levels of CB1-R.
- Apoptosis/drug effects
- Carcinogenesis/drug effects
- Cell Proliferation/drug effects
- Colonic Neoplasms/drug therapy
- Dietary Supplements
- Gene Expression/drug effects
- Mice, Inbred C57BL
- Proto-Oncogene Proteins c-bcl-2/metabolism
- Receptor, Cannabinoid, CB1/metabolism
- Up-Regulation/drug effects
- bcl-2-Associated X Protein/metabolism