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- W2373490020 abstract "AIM: To study the effects of macrocalyxin A(MA) on proliferation inhibition and apoptosis in HL-60 human leukemia cell line and explore its mechanisms.METHODS: Different concentrations of MA and different times of cultivation were used to treat HL-60 cell.The proliferation inhibition was analyzed by MTT assay.The cell apoptosis was analyzed by cell morphology,DNA agarose gel electrophoresis,DNA content and cell cycle analyzation,Annexin-V/PI and Hoechst 33258 fluorescence staining.The expressions of Bcl-2,Bax,Fas P53 and mitochondrial membrane protein were analyzed by flow cytometry,while the mitochondrial transmembrancepotential(ΔΨm) was labeled by dihydrorhodamin 123.RT-PCR method was used to study the Bcl-2,Bax,P53 and caspase-3 mRNA levels.RESULTS: MA could inhibit HL-60 cell proliferation viability within a certain range of treating time and dose,with a 24 h IC50 of 8.76 μg/mL,48 h of 7.17 μg/mL and 72 h of 7.14 μg/mL.A majority of HL-60 cells were arrested in G0/G1 phase.The HL-60 cells apoptosis was confirmed by type cell morphology,DNA fragment,sub-G1 phase and Annexin-Ⅴ/PI labeling method with a time and dose related manner.The expression of Bax was increased,and Bcl-2,P53 and fas were unchanged by the treatment of MA.MA could increase the expression of mitochondrial membrane protein and caspase-3 in a dose-dependent manner while the ΔΨm was reduced.CONCLUSION: MA can inhibit the proliferation and induce the apoptosis of HL-60 cells.The mechanisms associate with its up-regulation of Bax and the ratio of Bax/Bcl-2,decreasing the mitochondrial membrane potential,opening the mitochondrial membrane pore and activating caspase-3." @default.
- W2373490020 created "2016-06-24" @default.
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- W2373490020 date "2009-01-01" @default.
- W2373490020 modified "2023-09-23" @default.
- W2373490020 title "Macrocalyxin A induces apoptosis by mitochondrial signaling pathway in HL-60 leukemia cells" @default.
- W2373490020 hasPublicationYear "2009" @default.
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