›› 2012, Vol. 24 ›› Issue (1): 10-13.doi: 10.3969/j.issn.1004-616x.2012.01.003

• 论著 • 上一篇    下一篇

p38 MAPK在喹乙醇诱导HepG2细胞凋亡中的作用

赵文霞,张朝明,汤树生,张 婷,孙 雨,靳 溪,肖希龙   

  1. 中国农业大学动物医学院药理和毒理教研室,北京 100193
  • 收稿日期:2011-06-15 修回日期:2011-07-18 出版日期:2012-01-30 发布日期:2012-01-30
  • 通讯作者: 肖希龙

Effects of p38 MAPK signaling pathway on apoptosis stimulated by olaquindox in human hepatoma G2 cells

ZHAO Wen-xia,ZHANG Chao-ming,TANG Shu-sheng,ZHANG Ting,SUN Yu,JIN Xi,XIAO Xi-long   

  1. Department of Pharmacology and Toxicology, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China
  • Received:2011-06-15 Revised:2011-07-18 Online:2012-01-30 Published:2012-01-30
  • Contact: XIAO Xi-long

摘要: 目的: 研究p38 MAPK信号通路在喹乙醇诱导的HepG2细胞凋亡中的作用。方法:分别用不同浓度 (0、200、400、800 μg/ml)的喹乙醇染毒HepG2细胞24 h和800 μg/ml喹乙醇染毒HepG2细胞不同时间 (0、0.5、1、2、4、6、12、24 h)后,采用Western blot法检测细胞内磷酸化p38蛋白和p38总蛋白的表达情况,以p38 MAPK磷酸化水平反映p38 MAPK信号通路的活性。分别采用0、10、20 μmol/L的p38 MAPK特异性抑制剂SB203580预处理HepG2细胞1 h后,再用800 μg/ml喹乙醇染毒24 h,采用Annexin V-FITC/PI法检测细胞凋亡。结果:随着喹乙醇染毒浓度和时间的增加,HepG2细胞的p38磷酸化蛋白表达量逐步增加,其中800 μg/ml喹乙醇染毒细胞24 h的实验组与对照组相比,p38磷酸化蛋白的表达量明显上调 (P<0.01)。10、20 μmol/L的SB203580对喹乙醇诱导细胞凋亡有促进作用,细胞的凋亡率分别为35.4%±2.83%、40.2%±3.98%,较喹乙醇对照组 (23.1%±3.59%)明显升高 (P<0.05)。结论:喹乙醇能激活p38 MAPK信号通路,且p38 MAPK信号通路的激活参与抑制喹乙醇介导的HepG2细胞凋亡的过程。

关键词: 喹乙醇, p38 MAPK, 细胞凋亡, HepG2细胞

Abstract: OBJECTIVE: To investigate the effect of p38 MAPK signaling pathway on the apoptosis induced by olaquindox in human hepatoma G2 (HepG2) cells. METHODS:The HepG2 cells were treated with different concentrations (0,200,400,800 μg/ml) of olaquindox for 24 h or with 800 μg/ml olaquindox for different time points (0,0.5,1,2,4,6,12,24 h). Then the expression of p38 and phosphorylation of p38 (p-p38) were determined by Western blot. The HepG2 cells which were pretreated with different concentrations (0,10,20 μmol/L) of SB203580 for 1 h were subsequently treated with 800 μg/ml olaquindox for 24 h. The changes of apoptosis were analyzed by Annexin V-FITC and propidium iodide (PI) staining. RESULTS:The expression of p-p38 increased gradually with the dose and time of olaquindox treatment. Moreover,compared with control group,the expression of p-p38 was observably apparent with the treatment of 800 μg/ml olaquindox for 24 h (P<0.01). Compared with olaquindox control group (23.1%±3.59%),the apoptosis of olaquindox-treated HepG2 cells was enhanced by different concentrations (10,20 μmol/L) of SB203580 with the apoptotic rate of 35.4%±2.83% and 40.2%±3.98% respectively (P<0.05). CONCLUSION:p38 MAPK signaling pathway was activated by olaquindox,which played a role in inhibiting apoptosis induced by olaquindox-treated HepG2 cells.

Key words: Olaquindox, p38 MAPK, apoptosis, HepG2 cells