Prevention and treatment of colon cancer with pomegranates


The effect of pomegranate seed oil (PGO) was studied in mice on the occurrence of colonic aberrant crypt foci (ACF) induced by azoxymethane. Colonic tumors were induced in 6-week old male F344 rats by subcutaneous injections of AOM once a week for 2 weeks. One week before the AOM treatment, mice were started on a diet containing 0.01, 0.1, or 1% PGO for 32 weeks. After 32 weeks, the incidence of colon tumors was 81% with a tumor multiplicity of 1.88/mice.

Administration of PGO in the diet significantly inhibited the incidence and multiplicity of colonic adenocarcinomas; however, a dose-response relationship was not observed. The inhibition of tumor incidence was associated with increased expression of peroxisome proliferator-activated receptor (PPAR) gamma protein in the non-tumor mucosa. Rats received 20% pomegranate juice in drinking water and 3 weeks later received subcutaneous injections of AOM.

Total glutathione-S-transferase (GST) activity in the liver of the rats fed pomegranate juice was significantly higher compared with the control, suggesting that pomegranate juice contributes to significant reductions in the formation of AOM-induced ACF.

Some doctors examined the effects of pomegranate juice on inflammatory cell signaling proteins in HT-29 human colon cancer cell line based on the fact that inflammation plays a key role in the development of colon cancer. At a concentration of 50 mg/L, pomegranate juice significantly suppressed TNF alpha-induced COX-2 protein expression by 79% and also reduced phosphorylation of the NF-kB/p65 subunit and its binding to the NF-KB response element.

Pomegranate juice also abolished TNF alpha-induced AKT activation, needed for NF-KB activity. These data provided evidence that polyphenolic constituents in the pomegranate play an important role in the modulation of inflammatory signals in colon cancer cells.

Other doctors observed that the anti-carcinogenic effect of dietary elagitannins could be mainly due to their hydrolysis product, elagic acid. Punicalagin was hydrolysed in the medium to yield elagic acid which entered into the cells, was metabolised to produce dimethyl-elagic acid, which then induced apoptosis via mitochondrial pathway in colon cancer Caco-2 cells but not in normal colon cells.

Among several fruit juices tested (apple, peach, orange, pineapple, grapefruit, and pomegranate), pomegranate juice potently inhibited the sulfoconjugation of 1-naphthol in Caco-2 cells. Punicalagin, the most abundant antioxidant polyphenol in pomegranate juice, was also found to strongly inhibit sulfoconjugation in Caco-2 cells with an IC50 of 45 micro M. Phase II conjugation activity in the intestinal epithelium affects the bioavailability of drugs and other environmental xenobiotics. Pomegranate juice and punicalagin both inhibited phenol sulfotransferase activity in Caco-2 cells in vitro.

These results suggest that constituents of pomegranate juice, most probably punicalagin, impair the enteric functions of sulfoconjugation and that this might have effects upon the bioavailability of drugs and other compounds present in food and in the environment and further, the effects might be related to the anti-carcinogenic properties of pomegranate juice.

Components of Wnt signaling pathways are known to play a pivotal role in human colon carcinogenesis, and inappropriate activation of the signaling cascade is observed in 90% of colorectal cancers. Doctors investigated the effects of components of pomegranate extracts on Wnt signaling in a human 293T cell line using a luciferase reporter of canonical Wnt pathway-mediated transcriptional activation. The elagitannin extracts, ellagic acid, and urolithins inhibited Wnt signaling, suggesting that ET-rich foods have potential against colon carcinogenesis.

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