续断皂苷抗白血病作用的机制探讨

作者	单位
周鹏	苏州大学附属第一医院中心实验室
马亮	苏州大学附属第一医院中心实验室
周珺	苏州大学附属第一医院中心实验室
国风	苏州大学附属第一医院中心实验室

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中文摘要:

目的探讨续断皂苷(akebia saponinD,ASD)抗白血病细胞及其作用机制。方法用不同剂量(10、30、50、100μg/mL)皂苷处理人急性白血病细胞株U937细胞和人早幼粒白血病细胞株HL-60细胞,采用MTT比色法观察ASD对白血病细胞的作用。以Annexin-Ⅴ染色法检测细胞凋亡并以PCR法检测凋亡相关基因的表达。采用Westernblot法检测P53蛋白的变化。采用Griess分光光度法检测样品中一氧化氮(NO)的代谢产物亚硝酸盐的含量。结果与未处理组相比,50μg/mLASD能明显抑制U937细胞和HL-60细胞的生长并呈剂量依赖性,同时伴随bcl-2mRNA表达的明显下调。Western blot检测结果显示,P53蛋白的表达水平随ASD作用而升高。另外,ASD可以促使U937细胞和HL-60细胞中NO的含量显著提高(P<0.05)。结论 ASD对U937细胞和HL-60细胞具有增殖抑制和诱导凋亡的作用,其机制与bcl-2基因的下调,p53蛋白上调,以及促进白血病细胞内NO含量提高相关。

英文摘要:

Objective To investigate the mechanism of akebia saponin D(ASD) for fight against leukemia cells.Methods The human acute leukemia cell strain U937 and human acute promyelocytic leukemia cell strain HL-60 were treated with ASD at different doses(10,30,50,and 100 μg/mL).The proliferation inhibition of ASD was observed using MTT assay.Apoptosis was detected by Annexin-Ⅴ staining.The expressions of correlated genes were detected by PCR.Changes of p53 were detected using Western blot.The nitrite content,as the metabolite of nitric oxide(NO) was detected by Griess spectrophotometry.Results 50 μg/mL ASD could obviously inhibit the growth of U937 and HL-60 cells in a dose-dependent manner,accompanied with the down-regulation of bcl-2 mRNA expression.Results of Western blot showed that the P53 expression increased along with the dose of ASD.Besides,ASD could elevate the content of NO in U937 and HL-60 cells(P<0.05).Conclusions ASD could inhibit the proliferation and induce the apoptosis of U937 and HL-60 cells.The mechanism might be correlated with down-regulating the bcl-2 expression,up-regulating the p53 expression,and increasing the NO content in U937 and HL-60 cells.

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