Cilostazol inhibits expression of P38 mitogen-activated protein kinase and proliferation of human vascular endothelial cells
10.3760/cma.j.issn.1671-8925.2011.12.006
- VernacularTitle:西洛他唑对人血管内皮细胞增殖及P38MAPK表达的抑制作用
- Author:
Yan-Jun HUANG
1
;
Zhen-Hua LIU
;
Hui LIU
;
Hui-Fang XIE
Author Information
1. 南方医科大学珠江医院
- Keywords:
Cilostazol;
Vascular endothelial cell;
Cell proliferation;
Mitogen-activated protein kinase
- From:
Chinese Journal of Neuromedicine
2011;10(12):1211-1214
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect ofcilostazol(CLZ)on proliferation of human vein endothelial cells(VECs)in vitro and activity ofphosphorylation P38 mitogen-activated protein kinase (MAPK).Methods Human umbilical vein endothelial cell(HUVEC)line EA.hy926 culturedin vitro was treated with CLZ at concentrations of 10,30,100 and 300 μmo/L for 24 h; blank controls were also employed.The ratio of cell proliferation was determined by MTT assay; the protein expression of phosphorylation P38MAPK was evaluated by Western blotting.Results The proliferation ratio(A value)of HUVECs was(0.909±0.013)in the control group,and(0.903 ±0.026),(0.851 ±0.023),(0.699±0.013),and(0.651±0.036)in the 10,30,100 and 300 μno/L CLZ-treatment groups,respectively; as compared with that in the blank control group,the A value in the 30,100 and 300 μmo/L CLZ-treatment groups was significantly lower(P＜0.05); and a decreased trend at dose-dependent manner was noted among the 30,100 and 300 μno/L CLZ-treatment groups.As compared with that in the control group,the protein expression of phosphorylation P38MAPK in the 30,100 and 300 μmo/L CLZ-treatment groups was significantly decreased(P＜0.05),and the protein expression of phosphorylation P38MAPK in 300 μmo/L CLZ-treatment group was significantly lower than that in 30 μno/L CLZ-treatment group (P＜0.05).Conclusion CLZ can obviously inhibit the protein expression of P38MAPK and in vitro proliferation of VECs.
