title: [The effect of p38 on the cycloheximide-induced HL-60 cell death through mitochondria pathway].
abstract: OBJECTIVE
  To study the effect of p38 on the cycloheximide (CHX)-induced HL-60 cell death through mitochondria pathway.
  
  
  METHODS
  Inhibition of p38 pathway was by SB203580 (SB). Four groups were set up: control, SB only, CHX only and SB + CHX. Sub-diploid cell ratio was detected by PI staining flow cytometry at 6, 9, 12, 18, 24 h time points, and apoptotic cell ratio by Annexin V-FITC/PI double staining flow cytometry at 6 h and 18 h time points. High J-aggregate cells were evaluated by the J-aggregate contents, measurement of the J-aggregate (FL2) and J-monomer (FL1) by JC-1 flow cytometry, calculation of the delta psi m by FL2/FL1 and analysis of the delta psi m changes at 18 h time points.
  
  
  RESULTS
  The sub-diploid cell ratio in CHX group was significantly higher than that in control group at 6 h time point, and the ratio in SB + CHX group was significantly higher than that in CHX group at 9 h time point. At 18 h time point the apoptotic cell ratios in both CHX and SB + CHX groups were significantly higher than those in control group (P < 0.01). There was no significant difference of apoptotic cell ratio between CHX group and SB + CHX group (P > 0.05). At 18 h time point the necrotic cell ratios in both CHX and SB + CHX groups were significantly higher than that in control group (P < 0.01); and that in SB + CHX group was significantly higher than that in CHX group (P < 0.01). The high J-aggregate cell ratios in CHX and SB + CHX groups were significantly lower than that in control group (P < 0.05), and that was signficantly lower in SB + CHX group than in CHX group (P < 0.01). For the FL2/FL1 value (delta psi m) CHX group (0.17 +/- 0.01) and SB + CHX group (0.05 +/- 0.003) were significantly higher than control group (0.38 +/- 0.02) (P < 0.01), and SB + CHX group was significantly lower than CHX group (P < 0.01).
  
  
  CONCLUSIONS
  CHX can induce HL-60 cell apoptosis and the cell mitochondria depolarization, and the latter was intensified by inhibition of the p38 pathway. p38 pathway may related to the cell necrosis in the cycloheximide-induced HL-60 cell apoptosis model. s
authors.affiliation: Key Laboratory of Tissue Transplantation and Immunology of National Education Dept., Jinan University, Guangzhou 510632, China.
authors.forename: Pei-yan
authors.initials: PY
authors.lastname: Liang
authors.forename: Yao-ying
authors.initials: YY
authors.lastname: Zeng
authors.forename: Tong
authors.initials: T
authors.lastname: Wang
authors.forename: Fei-yue
authors.initials: FY
authors.lastname: Xing
authors.forename: Jing-xian
authors.initials: JX
authors.lastname: Zhao
authors.forename: Xun
authors.initials: X
authors.lastname: Jiang
authors.forename: Jing-fang
authors.initials: JF
authors.lastname: Di
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D003513:Cycloheximide / Q000494:pharmacology; D018922:HL-60 Cells; D006801:Humans; D008564:Membrane Potentials; D008928:Mitochondria / Q000502:physiology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D003513:Cycloheximide; D048051:p38 Mitogen-Activated Protein Kinases