DADS 诱导人 HepG2 细胞凋亡中 p38MAPK 和 caspase-3 的作用。

The roles of p38MAPK and caspase-3 in DADS-induced apoptosis in human HepG2 cells.

机构信息

College of Chemistry and Chemical Engineering, Central South University, Changsha, Hunan 410083, China.

出版信息

J Exp Clin Cancer Res. 2010 May 18;29(1):50. doi: 10.1186/1756-9966-29-50.

OBJECTIVES

To explore the function of p38MAPK and caspase-3 in DADS-induced apoptosis in human HepG2 cells, and discuss the signal transduetion mechanism of HepG2 cells in the apoptosis process induced by DADS by using the inhibitors of p38MAPK (SB203580) and caspase-3 (Z-DEVD-FMK).

METHODS

After the human HepG2 cells had been treated with the DADS and inhibitors for 24 h, cell viability was determined by the MTT method, apoptosis was evaluated by flow cytometry (FCM) and the expressions of p38MAPK and caspase-3 were measured by western-blot.

RESULTS

Our results indicated that DADS activities the p38MAPK and caspase-3, but the inhibitors, SB203580 and Z-DEVD-FMK (for p38MAPKand for caspase-3, respectively), both have the effect of inhibitory activity on P38MAPK and caspase-3. Furthermore, a combination treatment with both DADS and inhibitor (SB203580 or Z-DEVD-FMK) decreases the inhibitory and apoptotic activity of HepG2 cells increased compared with DADS-treated.

CONCLUSIONS

Our data indicate that p38MAPK and caspase-3 are involved in the process of DADS-induced apoptosis in human HepG2 cells and interact with each other.

目的

探讨 p38MAPK 和 caspase-3 在 DADS 诱导人 HepG2 细胞凋亡中的作用，并通过 p38MAPK（SB203580）和 caspase-3（Z-DEVD-FMK）抑制剂探讨 DADS 诱导 HepG2 细胞凋亡过程中的信号转导机制。

方法

用 DADS 和抑制剂处理人 HepG2 细胞 24 h 后，采用 MTT 法测定细胞活力，流式细胞术（FCM）检测细胞凋亡，Western blot 检测 p38MAPK 和 caspase-3 的表达。

结果

结果表明，DADS 激活了 p38MAPK 和 caspase-3，但抑制剂 SB203580 和 Z-DEVD-FMK（分别用于 p38MAPK 和 caspase-3）均对 p38MAPK 和 caspase-3 具有抑制活性。此外，与 DADS 处理相比，DADS 联合抑制剂（SB203580 或 Z-DEVD-FMK）治疗可降低 HepG2 细胞的抑制和凋亡活性。