雷公藤红素诱导人急性髓系白血病HL-60细胞凋亡及其机制的研究

Effect and possible mechanism of tripterine on inducing apoptosis of human acute myelocytic leukemia HL-60 cells

探讨雷公藤红素诱导人急性髓系白血病HL-60细胞凋亡的作用及其机制．采用台盼蓝染色法、透射电镜和流式细胞术，分别检测不同浓度和作用时间下，雷公藤红素诱导HL一60细胞凋亡以及对细胞Fas、FasL和NF-κBP65表达的影响．结果表明：0．5～2．5μmol·L^-1浓度雷公藤红素作用24h，HL-60细胞凋亡率均明显高于不加药物的对照组（P〈0．05）．当雷公藤红素浓度为1．5μmol·L^-1时，细胞凋亡率最高并呈时间依赖效应．雷公藤红素作用的HL-60细胞，可呈现典型的细胞凋亡形态学改变．1．5μmol·L^-1雷公藤红素可明显提高Fas和FasL阳性HL-60细胞百分率（P〈0．05），但抑制细胞NF—κBP65的表达（P〈0．05）．从而得出结论：雷公藤红素可有效地诱导HL-60细胞凋亡，其机制与雷公藤红素可上调Fas、FasL基因及下调NF—κB基因表达有关．

The effect and possible mechanism of tripterine on inducing human acute myelocytic leukemia HL-60 cell apoptosis were investigated. By using trypan-blue staining method, transmission electron microscopy （TEM）, and flow cytometry （FCM）, the effects of triperine with different dosages and durations to induce the apoptosis as well as the expression of Fas, FasL and NF-κBP65 of HL-60 cells were also studied. All the apoptic rates of HL-60 cells treated with 0.5-2.5μmol·L^-1 tripterine for 24 hours were remarkably higher than that with no drug treatment （P〈0.05）. When the used dosage of tripterine was 1.5 μmol·L^-1, the maximal apoptic rate could be found as a time-dependent pattern. Typical apoptlc morphological changes in the tripterine-treated HL-60 cells were found. Tripterine with a dosage of 1.5 μmol·L^-1 could increase the positive rates of Fas and FasL positve HL-60 cells （P 〈0.05）, but inhibit the expression of NF-κBP65 in the cells （P〈0.05）. Tripterine can efficiently induce the apoptosis of HL60 cells. The anti tumor mechanism of tripterine is probably involved to up-regulate the expression of Fas and FasL genes and to down-regulate the expression of NF-κB gene in the treated HL-60 cells.