Objective The purpose of this study was to determine the effect of quercetin on the antitumor activity of cisplatin and its side-effects. Methods EMT6 cells, a mouse breast cancer cell line, were injected subcutaneously in mice to generate a breast tumor-bearing mouse model. Experimental groups were divided into four groups: control (C), quercetin (Q), cisplatin (CP), and cisplatin+quercetin (CP+Q). Results The tumor volume of the CP+Q group was significantly lower than that of the CP group. Serum blood urea nitrogen and creatinine levels in the CP+Q group were lower than those in the CP group. Renal γ-glutamyltranspeptidase and alkaline phosphatase activities were significantly higher in the CP+Q group than in the CP group, and the content of renal thiobarbituric acid reactive substance was significantly lower in the CP+Q group than that in the CP group. These results suggested that quercetin and cisplatin synergistically increased cellular toxicity in breast cancer cells and mediated cancer growth inhibition, thereby enhancing the antitumor effect of cisplatin compared to when only cisplatin was administered. Quercetin also reduced renal toxicity, which arose as a potential a side effect of cisplatin. Conclusion The enhanced antitumor effect of cisplatin and decreased renal toxicity after quercetin treatment suggested the applicability of quercetin as an adjuvant for chemotherapeutic agents.

ObjectiveTo investigate the effect of genistein on the anticancer effects of chemotherapeutic agents, we examined the effect of a genistein and cisplatin combination on CaSki human cervical cancer cells.MethodsAfter the cervical cancer cells (HeLa cells, CaSki cells) had been cultured, cisplatin and genistein were added to the culture medium, and the cell activity was measured using MTT assay. The CaSki cells were cultured in a medium containing cisplatin and genistein, and then, the cells were collected in order to measure p53, Bcl2, ERK, and caspase 3 levels by western blotting.ResultsBoth the HeLa and CaSki cells had decreased cell viabilities when the cisplatin concentration was 10 μM or higher. When combined with genistein, the cell viabilities of the HeLa and CaSki cells decreased at cisplatin concentrations of 8 μM and 6 μM, respectively. The administration of genistein increased the toxicity of cisplatin in the HeLa and CaSki cells. In the CaSki cells, the p-ERK1/2 level decreased by 37%, the p53 expression level increased by 304%, and the cleaved caspase 3 level increased by 115% in the cisplatin+genistein group compared to that in the cisplatin group. Bcl2 expression was reduced by 69% in the cisplatin+genistein group compared to that in the cisplatin group.ConclusionGenistein enhances the anticancer effect of cisplatin in CaSki cells, and can be used as a chemotherapeutic adjuvant to increase the activity of a chemotherapeutic agent.

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Myocarditis induced by 5-aminosalicylic acid (ASA) is a rare and idiosyncratic adverse event requiring discontinuation of the drug. There have been very few cases of balsalazide induced myocarditis. Balsalazide is known to cause less complications compared to mesalamine due to its lower serum concentration. However, in the case of idiosyncratic adverse effects, clinicians should be aware that all 5-ASA drug have the potential to cause myocarditis in patients with ulcerative colitis (UC). We report a case of balsalazide induced myocarditis in a 26-year-old female patient with UC. She was treated UC with balsalazide and added topical mesalamine one month ago. Her myocarditis was improved by discontinuation of basalazide and topical mesalamine. We considered a recently added topical mesalamine as a cause of myocarditis. Although basalazide is 5-ASA, it was carefully re-introduction because it was previously well tolerable. Finally, balsalazide induced myocarditis was confirmed by recurrence of myocarditis.