摘要
目的:观察远志皂苷元诱导肺癌A549细胞凋亡作用,初步探讨其可能作用机制。方法:以肺癌A549细胞为实验对象,通过不同浓度的远志皂苷元(0、5、10、20、40、80μmol/L)处理A549细胞,MTT观察细胞增殖情况;Annexin V-FITC/PI双标法检测细胞的凋亡率;比色法检测半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)和半胱氨酸天冬氨酸蛋白酶-9(Caspase-9)的活性;Real Time PCR检测凋亡相关基因TNF-α、Bcl-2、Caspase-3和Survivin的表达。结果:远志皂苷元可显著抑制A549细胞增殖(P<0.05)、诱导A549细胞凋亡(P<0.05)。同时增强Caspase-3和Caspase-9的活性,显著改变TNF-α、Bcl-2、Caspase-3和Survivin的基因表达(P<0.05)。结论:远志皂苷元可诱导A549细胞凋亡,其机制可能与其调节Caspase家族因子活性有关。
Objective： To explore the effects and mechanism of senegenin on the induction of apoptosis in human pulmonary carcinoma cell A549. Methods： A549 cells were cultured in vitro and incubated with different concentrations of senegenin（0,5,10,20,40 and 80 μmol/L）. MTT method was used to make sure the inhibition of senegenin on the growth of A549 cells. Alteration of apoptosis rate of A549 cells was determined by Annexin FITC/PI double staining.Colorimetric assay was used to detect the activity of cysteine-aspartic acid protease 3（Caspase-3） and cysteine-aspartic acid protease 9（Caspase-9）. The expressions of TNF-α,Bcl-2,Caspase-3 and Survivin were determined by Real Time PCR. Results： Senegenin significantly inhibited the growth of A549 cells（P〈0. 05） and significantly induced the apoptosis on A549 cells（P〈0. 05） in a dose-dependent manner. The activities of Caspase-3 and Caspase-9were significantly improved（P〈0. 05）. The expressions of TNF-α,Bcl-2,Caspase-3 and Survivin were also significantly changed（P〈0. 05）. Conclusion： Senegenin could induce the apoptosis of A549 cells and its mechanism may be related to the activated Caspase family.
出处
《中华中医药学刊》
CAS
北大核心
2015年第9期2200-2203,共4页
Chinese Archives of Traditional Chinese Medicine
基金
浙江省公益性面上项目(2012YSB08)
