EFFECT OF NIMODIPINE ON Caspase SIGNAL PATHWAY OF HL-60 CELL APOPTOSIS INDUCED BY CYTARABINE
Yan-Xia Zhao
Abstract
Yan-Xia Zhao
Abstract
Objective To study the effect of nimodipine on the mechanism of HL-60 cell apoptosis induced by cytarabine(Ara-c). MethodsThe log phase HL-60 cells were collected,and divided into control group(no any drugs were aided),nimodipine group(0.001-0.100 g/L),Ara-c group(0.005-0.500 g/L) and nimodipine +Ara-c group.The cells in each group were treated for 24 h.ATP chemiluminometry was employed to detect the cell cytostasis and Caspase 8 activity in each group,and AO/EB fluorescent staining to observe the cell apoptosis. ResultsCompared with the control group,the differences of cell proliferation inhibition(PI) rate of HL-60 in different-concentration nimodepine or Ara-c groups were significant(F=12 231.563,6 404.210;P0.01).When the concentration of nimodepine was 0.050 g/L and that of Ara-c was 0.010 g/L,the PI rate being the highest(F=916.836,P0.01).When the concentration of Ara-c was 0.010 g/L,and that of nimodepine was 0.050 g/L,the cell apoptosis rate in both Ara-c and NMDP+Ara-c groups was dramatically higher that that in the control group and nimodepine group,the apoptosis being the highest in NMDP+Ara-c group(F=148.02,P0.01).Compared with the control and nimodipine,the activity of Caspase 8 in Ara-c group and NMDP+Ara-c group was enhanced,of which,the highest was seen in NMDP+Ara-c group(F=732.84,P0.01). ConclusionNimodipine can strengthen HL-60 cell apoptosis induced by Ara-c,the mechanism is probably associated with enhancement of Caspase 8 activity.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To study the effect of nimodipine on the mechanism of HL-60 cell apoptosis induced by cytarabine(Ara-c). MethodsThe log phase HL-60 cells were collected,and divided into control group(no any drugs were aided),nimodipine group(0.001-0.100 g/L),Ara-c group(0.005-0.500 g/L) and nimodipine +Ara-c group.The cells in each group were treated for 24 h.ATP chemiluminometry was employed to detect the cell cytostasis and Caspase 8 activity in each group,and AO/EB fluorescent staining to observe the cell apoptosis. ResultsCompared with the control group,the differences of cell proliferation inhibition(PI) rate of HL-60 in different-concentration nimodepine or Ara-c groups were significant(F=12 231.563,6 404.210;P0.01).When the concentration of nimodepine was 0.050 g/L and that of Ara-c was 0.010 g/L,the PI rate being the highest(F=916.836,P0.01).When the concentration of Ara-c was 0.010 g/L,and that of nimodepine was 0.050 g/L,the cell apoptosis rate in both Ara-c and NMDP+Ara-c groups was dramatically higher that that in the control group and nimodepine group,the apoptosis being the highest in NMDP+Ara-c group(F=148.02,P0.01).Compared with the control and nimodipine,the activity of Caspase 8 in Ara-c group and NMDP+Ara-c group was enhanced,of which,the highest was seen in NMDP+Ara-c group(F=732.84,P0.01). ConclusionNimodipine can strengthen HL-60 cell apoptosis induced by Ara-c,the mechanism is probably associated with enhancement of Caspase 8 activity.
Key concepts: Apoptosis, Nimodipine, Cytarabine, Chemistry, Pharmacology, Molecular biology, Medicine, Internal medicine