ABSTRACT
Objective To investigate the mechanism of rosiglitazone on human leukemia cell line HL-60 in vitro.Methods Inhibition of HL-60 cell proliferation was shown by MTT array;cell cycle and apoptosis of human leukemia cell line HL-60 was detected by flowcytometry(FCM);expression of PPAR?,p21WAF1,Bax and bcl-2 was examined by SP immnocytochemical and western blotting.Results Rosiglitazone significantly inhibited proliferation of HL-60 cell and the inhibition effects had a dose-and time-dependence.The inhibition fraction of HL-60 cell to 100?mol/L rosiglitazone for 48h was 77%.Flow cytometry analysis revealed that proliferation of HL-60 cell treated with 10~100?mol/L rosiglitazone significantly inhibited.50~100?mol/L Rosiglitazone cold induce apoptosis of HL-60 cell.SP immnocytochemical found the nuclear translocation on PPAR?,and western blotting revealed that the Bax expression was increased,while the bcl-2 and NF-?B expression was decreased.The expression of PPAR?,Bax,bcl-2 and NF-?B had no change by GW9662,a specific inhibitor of PPAR?.Conclusion Rosiglitazone could induce apoptosis in HL-60 cells which may be involved in the activation of PPAR? and down-regulation of Bax and up-regulation of Bcl-2 and NF-?B protein.
ABSTRACT
Aim To investigate the differential expression of apoptosis-associated genes in human gastric cancer MGC803 cells induced by diallyl trisulfide(DATS).Methods Growth inhibition against MGC803 cells was assayed by MTT assay;The apoptosis induced by DATS was assessed by Flow cytometry and fluorescent microscope.The apoptosis-associated gene expression of MGC803 cell treated with DATS was determided by Human Apoptosis Gene Array.Apaf-1 and SODD genes were confirmed by RT-PCR.Results DATS had significant growth inhibitory activity against MGC803 cells,inhibition ratio increased from 11% to 78% at 4,8,12,16 and 24 mg?L-1 for 72 h(P