摘要
目的探讨丹皮酚对人卵巢癌SKOV3细胞的促凋亡作用及其可能的机制。方法用25、50、100、200、400μg/ml丹皮酚处理SKOV3细胞,设未经丹皮酚处理的细胞为对照组,24 h后,采用MTT法检测细胞增殖情况;用50、100、200μg/ml丹皮酚处理SKOV3细胞,设未经丹皮酚处理的细胞为对照组,24 h后,采用流式细胞术(flow cytometry,FCM)、Hoechst染色法检测细胞凋亡情况,Western blot法检测caspase3及survivin蛋白的表达情况。结果与对照组相比,各浓度丹皮酚对SKOV3细胞的增殖均有明显的抑制作用,呈浓度依赖性(P<0.05),IC50值为200.06μg/ml;100、200μg/ml浓度组中SKOV3细胞凋亡率分别为(35.33±1.32)%、(39.56±1.27)%,与对照组[(9.01±1.21)%]相比明显增加(P<0.05);丹皮酚100、200μg/ml浓度组中发生凋亡的细胞数量较对照组多;丹皮酚处理后细胞凋亡相关蛋白survivin表达降低,而caspase3表达增加,高浓度组与低浓度组相比,差异均有统计学意义(P<0.05)。结论丹皮酚能显著抑制人卵巢癌SKOV3细胞增殖,促进细胞凋亡,其机制可能与其调控凋亡相关蛋白survivin、caspase3表达变化有关。
Objective To investigate the promoting effect ot paeonol on apoptosls ol human ovarian cancer 31kUV3 cells as well as the possible relevant mechanism. Methods SKOV3 cells were treated with paeonol at concentrations of 25, 50, 100, 200 and 400 μg/ml respectively for 24 h, and measured for proliferation level by MTT assay, using those un- treated as control. In addition, the cells were treated with 50, 100 and 200 μg/ml paeonol for 24 h, then determined for apoptosis by flow cytometry （FCM） and Hoechst staining, and for expressions of caspase3 and survivin by Western blot, using those untreated as control. Results The proliferation of SKOV3 cells was inhibited by paeonol in a dose-dependent manner （P 〈 0. 05）, with an ICs0 of 200. 06 μg/ml. The apoptosis rates of SKOV3 cells treated with paeonol at concen- trations of 100 and 200 Ixg/ml were （35. 33 ± 1.32）% and （39. 56 ± 1.27） % respectively, which were significantly higher than those in control group [（9. 01 ± 1.21 ） %, P 〈 0. 051. The number of apoptotic cells treated with 100 and 200 μg/ml paeonol was larger than that in control group. The expression level of survivin in SKOV3 cells treated with paeonol decreased, while that of caspase3 increased, which showed significant difference in high and low concentration paeonol groups （P 〈 0. 05 ）. Conclusion Paeonol inhibited the proliferation and promoted the apoptosis of human ovari- an cancer SKOV3 cells, of which the mechanism might be related to the regulation of expressions of apoptosis-associated proteins survivin and caspase3.
出处
《中国生物制品学杂志》
CAS
CSCD
2013年第10期1454-1457,共4页
Chinese Journal of Biologicals
