Study on mechanism of mitochondrial in K562/G01 cells apoptosis induced by triptolide
10.3760/cma.j.issn.1009-9921.2014.07.005
- VernacularTitle:雷公藤甲素诱导K562/G01细胞凋亡的线粒体机制研究
- Author:
Xiaofeng LIU
;
Liangming MA
;
Yujin LU
;
Bo BAI
- Publication Type:Journal Article
- Keywords:
Triptolide;
K562/G01 cells;
Mitochondria;
Apoptosis;
Cytochromes C
- From:
Journal of Leukemia & Lymphoma
2014;23(7):397-400
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the possible mechanism of mitochondrial in chronic myeloid leukemia cells K562/G01 cells apoptosis induced by triptolide.Methods K562/G01 cells were treated with different concentrations of triptolide.MTT assay was used to assess cytotoxic effect.FCM was used to determine apoptosis rate,mitochondrial membrane potential and the activity of Caspase-9 of each experimental group.Real-time quantitative PCR assay was used to quantify mRNA levels of Caspase-9 and cytochrome C and Western blot assay was used to determine protein levels of cytochrome C.Results Triptolide inhibited the growth and proliferation of K562/G01 cells in a time-and dose-dependent manner (both P ＜ 0.001).Meantime,triptolide could make the mitochondria membrane potential fade away and enhance the activity of Caspase-9 (F =566.431,2 555.485,P ＜ 0.001).In addition,triptolide could dose-dependently up-regulated the transcription of Caspase-9 and cytochrome C (F =61 007.702,452 121.760,P ＜ 0.001),and the protein expression of cytochrome C,whose gray value in each experimental group was 21.54±0.59,39.63±0.58,53.29± 1.47 and 75.68±1.87 (F =5 677.928,P ＜ 0.001) respectively.Conclusion Triptolide could potently inhibit the growth and proliferation of K562/G01 cells,and the mitochondria apoptosis pathway might be one of the important apoptosis mechanisms in chronic myeloid leukemia cells induced by triptolide.
