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Xanthohumol, the principal flavonoid in hops, was investigated for its radiosensitizing activity on human cancer cells (human breast cancer MCF‐7 and ardiamucin‐resistant MCF‐7 (MCF‐7/ADR) cells, and human colon cancer HT‐29 and HCT116 cells). Cell survival was measured by the MTT assay 2 days after 10 Gy of ionizing radiation. Cells expressing mutant p53 (MCF‐7/ADR and HT29) are more resistant to the ionizing radiation than wild‐type p53 cells (MCF‐7 and HCT116). However, pretreatment of the cells with xanthohumol (10 μM) for 24 h prior to the radiation significantly enhanced radiosensitivity of all the cells, irrespective of p53 status. Some studies showed that there is persistent activation of signal transducer and activator of transcription 3 (STAT3) in a number of human solid tumors including colon cancer. In addition, MCF‐7/ADR showed persistent activation of STAT3. Xanthohumol significantly suppressed the expression of STAT3. In the cells co‐treated with xanthohumol and radiation could have the therapeutic potential as a radiosensitizer in human cancer cells overexpressing STAT3.

In inflammatory bowel disease (IBD), colon epithelial cells increased the expression of a variety of inflammatory mediators, cell adhesion molecules and chemokines. In this study, we examined the effect of novel propenone derivatives, 1,3‐diphenyl‐propenone (DPhP), 3‐phenyl‐1‐thiophen‐2‐yl‐propenone (PhT2P), 3‐phenyl‐1‐thiophen‐3‐yl‐propenone (PhT3P) and 1‐furan‐2‐yl‐3‐phenyl‐propenone (FPhP), on inflammatory cytokine‐induced responses in HT‐29 human colon epithelial cells. We found that DPhP most effectively blocked TNF‐α‐induced adhesion of U937 monocytes to HT‐29 cells, which is an initial step of colon inflammation. DPhP inhibited the expression of IL‐8, MCP‐1 and ICAM‐1 in a concentration‐dependent manner. When HT‐29 cells were transfected with NF‐κB‐Luc plasmid, DPhP significantly inhibited TNF‐α‐induced luciferase activity. In trinitrobenzene sulfonic acid (TNBS)‐induced rat colitis model, DPhP dose‐dependently protected from the TNBS‐induced weight loss, myeloperoxidase activity increase. At the same time, DPhP suppressed the TNBS‐induced mRNA expression of IL‐8, IL‐6 and MCP‐1. Taken together, the results suggest that DPhP may be a potential candidate to suppress the colon inflammation via inhibition of major pro‐inflammatory cytokines involved in intestinal inflammation.