芹菜素敏化TRAIL诱导人卵巢癌CoC1细胞凋亡

Sensitization of Human Ovarian Cancer CoC1 Cells to TRAIL-induced Apoptosis by Apigenin

目的:研究芹菜素(API)是否具有敏化肿瘤坏死因子相关凋亡诱导配体(TRAIL)诱导人卵巢癌CoC1细胞凋亡作用。方法:体外培养CoC1细胞。碘化丙啶(PI)染色流式细胞术(FCM)定量分析sub-G1细胞百分率。ELISA法测定细胞Caspase-3活性。结果:API(20μmol/L)和TRAIL(20ng/mL)以及两者合用48h的sub-G1细胞百分率分别是8.83%±2.33%、8.32%±2.80%和69.50%±4.65%;人卵巢癌CoC1细胞Caspase-3的活性分别是培养基组的1.3、1.4和6.5倍。结论:亚细胞毒性浓度的芹菜素具有增强TRAIL诱导人卵巢癌CoC1细胞凋亡作用。

Objective To investigate whether apigenin(API) sensitizes human ovarian cancer CoC1 cells to apoptosis induced by recombinant human soluble TNF-related apoptosis-inducing ligand(TRAIL).Methods Human ovarian cancer CoC1 cells were cultured in vitro.The percentage of sub-G1 cell population was determined by flow cytometry using PI fluorescence staining.Caspase-3 activity was determined using ELISA assay.Results Flow cytometry(FCM) analysis after PI stainning indicated that the percentage of sub-G1 cell population in human ovarian cancer CoC1 cells by API(20μmol/L) or TRAIL(20ng/mL) or both for 48h were 8.83%±2.33%,8.32%±2.80% and 69.50%±4.65%,respectively.Caspase-3 activity in CoC1 cells treated with 20 μmol/L API or 20ng/mL TRAIL or both for 48h was 1.3,1.4,6.5 fold in comparison with medium group.Conclusion API at subtoxic concentration sensitizes induction of apoptosis by TRAIL in human ovarian cancer CoC1 cell line.