Effect of ERK inhibition on the mitochondrial potential change in dexamethasone-induced thymocyte apoptosis
- VernacularTitle:阻断ERK途径对地塞米松诱导胸腺细胞凋亡中线粒体膜电势的影响
- Author:
Tong WANG
;
Yaoying ZENG
;
Peiyan LIANG
;
Feiyue XING
;
Wenting LUO
;
Xun JIANG
- Publication Type:Journal Article
- Keywords:
Dexamethasone;
Thymocytes;
Apoptosis;
Mitochondria;
Mitogen-activated protein kinases
- From:
Chinese Journal of Pathophysiology
1986;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To study the effect of ERK inhibition on the mitochondrial potential change in dexamethasone (DEX)-induced thymocyte apoptosis. METHODS: ERK activity was inhibited by PD098059 (PD), and 4 experimental groups were set: control, PD only, DEX and PD+DEX. Annexin V-FITC/PI double staining flowcytometry was used to detect apoptotic cells at time points of 3 h, 5 h and 7 h. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (△?m) at time points of 3 h, 7 h and 11 h. RESULTS: By stimulation with 1 ?mol/L DEX, the apoptotic rates of mouse thymocytes at 3 h, 5 h and 7 h were (19.63?0.35)%, (41.84?1.67)% and (67.00?2.43)%, respectively, and had significantly difference from control group (4.98?0.39)%, (6.08?0.33)% and (9.31?0.34)% (P0.05). At 3 h, 7 h and 11 h, the rates of low △?m cells were (21.23?1.43)%, (55.34?1.78)% and (70.88?2.87)%, significantly higher than that in control group (P0.05). CONCLUSION: DEX induces mouse thymocyte apoptosis at least partly through ERK pathway, and ERK inhibition has an important biological significance during this process.