达那唑抑制SKM-1细胞活性并促使细胞凋亡

Danazol inhibits cell viability and promotes apoptosis in SKM-1 cells

目的研究达那唑对骨髓增生异常综合征(myelodysplastic syndrome,MDS)细胞系SKM-1细胞活性、凋亡以及肿瘤坏死因子相关凋亡诱导配体(TNF-related apoptosis-inducing ligand,TRAIL)信号通路的影响。方法用0、10、20和40μmol/L达那唑处理SKM-1细胞后,通过MTT法检测细胞活性,通过流式细胞实验分析细胞周期和细胞凋亡,通过TUNEL染色法检测TUNEL阳性细胞比例,通过Western blot检测TRAIL介导的细胞凋亡相关蛋白的表达情况。结果达那唑可呈浓度依赖性地抑制SKM-1细胞活力,降低S期中细胞比率,提高细胞凋亡比率。Western blot结果显示达那唑可使Cleaved caspase-8和Cleaved PARP1水平升高。结论达那唑可抑制SKM-1细胞活性并促进其凋亡,其机制可能与激活TRAIL信号通路相关。

Objective To study the effect of danazol on the cell viability and apoptosis of SKM-1 cell line of myelodysplastic syndrome(MDS)and its impact on TNF related apoptosis inducing ligand(TRAIL)signal pathway.Methods SKM-1 cells were treated with 0,10,20 and 40μmol/L danazol,then the cell viability was detected by MTT assay,the cell cycle and apoptosis were analyzed by flow cytometry,the proportion of TUNEL positive cells was detected by TUNEL staining,and the expression of TRAIL-mediated apoptosis related proteins were detected by Western blot.Results Danazol inhibited cell viability,decreased the ratio of cells in S phase,and increased the apoptotic rate of SKM-1 cells in a concentration dependent manner.Western blot showed that danazol increased Cleaved caspase-8 and Cleaved PARP1 expression.Conclusion Danazole can inhibit the cell viability and promote the apoptosis of SKM-1 cells,and the mechanism may be related to the activation of TRAIL signaling pathway.