Effect Of Carotenoids And Quercetin On K562 Cell Proliferation And Pparγ Protein Expression

A growing body of evidence suggests that carotenoids have significant effects on antioxidant potential. And the further evidence from cell culture and animal experiments suggests thatβ-carotene, a carotenoid with the greatest pro-vitamin A activity, could be a compound responsible for the prevention and treatment of cancer.Quercetin(3,3',4',5,7-pentahydroxyflavone) is a naturally occurring flavonoid found in all aerial plants. In recent years, it was found to poss a variety of biological activities, such as antitumor, antioxidation, antiviral, lowering blood pressure, anti-arrhythmia, anti-platelet aggregation,and etc. Meanwhile, few side effects have been reported.Peroxisome proliferator-activated receptorγ(PPARγ) is a nuclear hormone receptor that plays a key role in the differentiation of adipocytes. Previous studies suggested that activation of this receptor in liposarcomas and breast cancer cells also induced cell growth inhibition and differentiation.In this study, leukemia cell line K562 cells were used as target cells. The inhibition of carotenoids and quercetin on proliferation of K562 cells and the effect on the expression of PPARγprotein were investigated. Also the mechanism underlying this relationship between carotenoids and quercetin and cancer cell proliferation was discussed.K562 cells were treated with different concentrations ofβ-carotene, bixin, capsanthin and quercetin (0.5μmol/L, 1.0μmol/L, 5.0μmol/L, 10.0μmol/L, and 20.0μmol/L) . The growth curve of K562 cells was detected by staining with trypan blue for viable cells counts with a haemacytometer. The inhibition of K562 cell proliferation was evaluated by the MTT test. The expression of PPARγin K562 cells was examined by western-blotting at protein level.The results showed that the K562 cell growth rate in carotenoids and quercetin treatment groups were slower than control group. With the increase of treatment time, the living cell numbers in bixin, capsanthin, and quercetin treatment groups were gradually reduced. The proliferation of K562 was obviously inhibited in a dose-dependent manner. Futhermore, the changes in cell morphology, as indicated by reduced living cells, different cell size, irregular shapes, and a lot of nuclear fragmentation, were apparent after carotenoid and quercetin treatment. The results of MTT test also showed that carotenoids and quercetin remarkably decreased the viability of K562 cells in dose- and time-dependent manners. The results of Western-blotting showed thatβ-carotene, capsanthin, bixin, and quercetin could up-regulate the expression of PPARγand may induce the apoptosis of the cells accordingly.According to these results, it were reasonable to infer that the up-regulation of PPARγexpression may contribute to the antiproliferative effects ofβ-carotene, capsanthin, bixin, and quercetin on K562 cells, among which carotenoids and quercetin may play a role as nonspecific ligands.