摘要目的 观察芹菜素(API)对雄激素非依赖前列腺癌PC-3细胞的调控作用并探讨其机制.方法 以不同浓度(0、10、20、40 μmol/L)的API干预PC-3细胞48 h,通过细胞形态学观察以及细胞计数试剂盒(CCK-8)法检测API对PC-3细胞的增殖抑制作用,逆转录-聚合酶链反应(RT-PCR)法检测半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3 mRNA的表达.结果 CCK-8法检测显示0、10、20、40μmol/L API处理PC-3细胞48 h后的吸光度值分别为1.48 ±0.04、0.81 ±0.04、0.69±0.03、0.33±0.03,相较于对照组,10、20、40 μmol/L API浓度组对PC-3细胞均有显著的增殖抑制作用,抑制率分别为44.7％、53.5％、77.4％ (P＜ 0.01).0、10、20、40 μmol/L API浓度组Caspase-3 mRNA的表达分别为0.230±0.036、0.410±0.080、0.480 ±0.100、0.730±0.150,实验组与对照组之间的差异均有统计学意义(P＜0.01).结论 API对PC-3细胞的增殖抑制作用呈剂量依赖性,其机制可能通过诱导PC-3细胞Caspase-3表达的增加,最终导致细胞凋亡.

abstractsObjective To observe the effect of apigenin (API) on the proliferation of human androgen-independent prostate cancer cell line PC-3 and molecular mechanisms.Methods Clutures of PC-3 cell were exposured to API at the different concentrationa of 0,10,20 and 40 μmol/L respectively.The effect of API on growth inhibition were determinated with morphometry,cell counting kit-8 (CCK-8) assay.The expression of Caspase-3 mRNA was determined by reverse transcriptase-polymerase chain reaction (RT-PCR).Results CCK-8 assay showed that the absorbance were 1.48 ±0.04,0.81 ±0.04,0.69 ± 0.03 and 0.33 ± 0.03 respectively when 0,10,20,40 μmol/L API treated PC-3 cells for 48 h,compared to the control group,10,20,40 μmol/L groups significantly inhibited the proliferation on PC-3 cells,the inhibition rates were 44.7％,53.5％,77.4％ (P ＜ 0.01).The Caspase-3 mRNA expression of 0,10,20,40 μmol/L group were 0.230 ± 0.036,0.410 ± 0.080,0.480 ± 0.100,0.730 ± 0.150,there was statistically significant differences between experimental and control groups (P ＜ 0.01).Conclusion The growth inhibition could be taken by API in PC-3 in a dose-dependent manner.The mechanism was that high expression level of Caspase-3 was caused by API,which led to the apoptosis of PC-3.