5-amino Imidazole-4-formamide Nucleotide United Interferon Effect On K562Cells

Objective：To investigate adenosine monophosphate kinase (AMPK) agonists5-amino-imidazole-4-carboxamide nucleotide (AICAR) in combination with interferon(IFN-a-2b) for chronic myeloid leukemia K562cell proliferation、 differentiation、apoptosis, to explore effect of possible mechanism.Methods：Detect cell proliferation condition with CCK8method；staining with themathod of Wright Giemsa, survey cell morphology; Flow cytometry instrument to detectdifferentiation antigen CD7, CD11b, CD34, HLA-DR expression; FITC Annexin V/PIdouble dye detection cell early apoptosis rate; Immunocytochemistry method to detectthe expression of wild-type P53protein.Results:1.Different concentration AICAR in different time of24h,48h,72h are inhibition ofK562cells, the degree of inhibition is time and dose dependent。2.AICAR combined IFN-a-2b can inhibit the growing of K562cells effectively.Combined72h the rate of cell inhibition reach to39.8%, compared with the controlgroup and AICAR alone and single with IFN-a-2b, there were virous statisticallysignificant in the differences (P <0.05).3.The combination of two drugs promote the expressi of wild-type p53protein level.4. The tendency for2.0mmol/L ICAR dealing with3days of K562cells comparedwith control group, the expression of CD7, CD11b, CD34, HLA-DR differentiationantigen stage on cell surface characteristics was no significant difference. cells obviousundifferentiated. Prompt AICAR did not show obvious role in inducing differentiation ofK562cells. Conclusion:1. AICAR and (or) INF-ɑ-2b could inhibit the proliferation of K562cells and at thesame time can promote it to apoptosis.2.The proliferation inhibition of AICAR effected on K562cell is in time and dosedependent.3. AICAR can have the effect of inhibit K562cells growthing, promote it to apoptosis.butthere is no evident impact to its differentiation.4. AICAR combined IFN-a-2b than single AICAR, IFN-a-2b more significantly inhibitproliferation,more promote apoptosis of K562cells.two-drug combination havesynergistic anti-tumor effect and its mechanism may be involve of raised the level ofP53protein with wild-type...