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目的探讨杭白菊与阿克拉霉素联合应用对白血病HL-60细胞诱导凋亡作用及机制。方法实验分组:(1)空白对照组,(2-4)不同浓度阿克拉霉素(0.05μg/ml、0.10μg/ml、0.25μg/ml)处理HL-60;(5)高浓度(500μM)的杭白菊处理;(6-8)不同浓度的杭白菊(10μM、100μM、500μM)与阿克拉霉素(0.1 g/ml)联合处理。20 h后流式细胞技术检测凋亡率,用Western blot分析COX-2、caspase 3、caspase 9和NF-κB蛋白表达。结果不同浓度阿克拉霉素诱导的凋亡率与空白组相似(P>0.05);不同浓度的杭白菊与阿克拉霉素联合处理,凋亡率明显增加(P<0.01)。杭白菊联合阿克拉霉素时caspase 3、caspase 9的表达明显升高,Cox-2和NF-κB的活性明显被抑制,与杭白菊浓度成正比(P<0.01)。结论杭白菊增强阿克拉霉素对HL-60细胞的诱导凋亡作用,以及抑制COX-2和增强caspase 3、caspase 9的表达,这是通过杭白菊增强对NF-κB活性的抑制作用而实现的。
Aim To investigate the apoptosis-inducing effect of Chrysanthemum morifolium and aclacinomycin on HL-60 leukemia cells and its mechanism. Methods The experimental groups were as follows: (1) blank control group, (2-4) HL-60 treated with different concentrations of aclacinomycin (0.05μg / ml, 0.10μg / ml and 0.25μg / ml) ); (6-8) different concentrations of chrysanthemum (10μM, 100μM, 500μM) and aclacinomycin (0.1 g / ml) combined treatment. After 20 h, the apoptosis rate was detected by flow cytometry. The expressions of COX-2, caspase 3, caspase 9 and NF-κB protein were detected by Western blot. Results The rates of apoptosis induced by aclacinomycin were similar to those of the blank group (P> 0.05). The apoptosis rates of chrysanthemum and aclacinomycin were significantly increased (P <0.01). When Chrysanthemum combined with aclacinomycin, the expression of caspase 3 and caspase 9 were significantly increased, and the activities of Cox-2 and NF-κB were significantly inhibited, which were directly proportional to the concentration of Chrysanthemum (P <0.01). Conclusion Chrysanthemum enhances the inducing apoptosis of HL-60 cells induced by aclacinomycin, as well as inhibits the expression of COX-2 and enhances the expression of caspase 3 and caspase 9, which is achieved through the inhibitory effect of chrysanthemum on the activity of NF-κB of.