| Carotenoids are a large class of tetraterpenes compounds by means of carbon atoms having alternate link of single bonds and double bonds as the centre frame. They not only are natural pigments, but also play important roles in human health and nutrition, such as, antioxidant and anticancer roles. And strong evidence suggests that diets rich in carotenoids can prevent the onset of some chronic diseases, such as preventing, delaying, and treating ischemic heart diseases, some tumors, immunodeficiency, aging, cataract, and light sensitive diseases. The supplemental and clinical applications ofβ-carotene which has the greatest provitamin A activity and been most widely used as a coloring agent and micronutrient in food have got accredits from the experts of WHO, EEC, FDA, and Japan. Carotenoids can induce the communication among cells. This is able to lead to the inhibitory effect of the proliferation of transforming cells, but also to the inhibitory effect of the growth of some tumor cells, such as breast cancer, adenocarcinoma, neurokeracele and leukemia cells(HL-60). A great deal of interest has been given to the understanding of the mechanisms of action by which carotenoids may modulate physiological functions and influence cell growth. It has been shown that carotenoids can inhibit the growth of chronic myelocytic leukemia(CML) cells, but little is known about the molecule mechanisms of action of carotenoids.The peroxisome proliferators-activated receptors (PPARs) are well-characterized transcription factors that are members of the nuclear hormone receptor superfamily. There are three PPARs subtypes (PPARα, PPARγ, and PPARδ). Relationship between PPARγand cancers has been paid attention to recently. It has been reported that the expression of PPARγis up-regulated in many tumor cells. PPARγis an important target for the development of new drugs aimed at preventing and treating cancer. Ligands for PPARγsuppress carcinogenesis in experimental models and induce the differentiation and apoptosis of human tumorigenic cells. There is as yet no report about whether carotenoids induce the expression of PPARγin leukemic K562 cells.The inhibitory action of carotenoids on growth of leukemic K562 cells and the effect of the expression of PPARγprotein were investigated in this paper.β-Carotene, capsanthin, canthaxanthin, and crocin were chosed to treat the cells. The inhibitory effect of K562 cell proliferation was detected by trypan blue dye exclusion method for viable cell counts with a haemacytometer.. The viability of K562 cells was evaluated by the MTT test. Apoptosis induced by the carotenoids was studied by a double staining method using FITC-conjugated annexin V and PI, and flow cytometry analysis.The expression of PPARγprotein was detected through Western blot analysis ( rabbit polyclonal anti-human PPARγantibody as a primary antibody ). GW9662, antagonist of PPARγ, was used to influence the cell growth for understanding the relationship between the regulation of PPARγexpression and the antoproliferation of carotenoids.The results showed that 6-carotene, capsanthin, and canthaxanthin can inhibit the growth of K562 cells in dose- and time-dependent manners except for crocin. The results of MTT test also showed thatβ-carotene and capsanthin remarkably decreased the viability of K562 cells. It was observed in our experiment thatβ-carotene and capsanthin were able to up- regulate the expression of PPARγat protein level in a dose-dependent manner. GW9662 can retrieve partly the viability of K562 cells decresed by carotenoids. From these results it was concluded thatβ-carotene and capsanthin was able to inhibit the proliferation of K562 cells by inducing apoptsis. The regulation of the expression of PPARγprotein may have some relation to the antiproliferative effect byβ-carotene and capsanthin, among which carotenoids may play a role as nonspecific agonists of PPARγ. |
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