| 李文海1 胡运生2 周勇安1 雷杰1 苏凯1 李小飞.水飞蓟宾诱导肺腺癌Anip973 细胞凋亡的分子机制研究[J].,2011,11(9):1670-1674 |
| 水飞蓟宾诱导肺腺癌Anip973 细胞凋亡的分子机制研究 |
| Molecular Mechanism of Sliybinin-induced Apoptosis of Lung CancerCell Anip973 |
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| DOI： |
| 中文关键词: 水飞蓟宾 肺癌细胞系Anip973 细胞凋亡 caspase |
| 英文关键词: Sliybinin Lung cancer cell Anip973 Apoptosis Caspase |
| 基金项目: |
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| 中文摘要: |
| 目的：探讨水飞蓟宾诱导肺腺癌Anip973 细胞系细胞凋亡的分子机制。方法：采用MTT 法、倒置显微镜和电子显微镜等形
态学检测以及流式细胞仪(FCM) 技术检测、DNA Ladder 分析、凋亡分子PARP 的表达检测细胞凋亡，同时进行凋亡相关蛋白
Bax、Bcl-2、caspase-3 和caspase-9 表达活性分析。结果：(1) 水飞蓟宾对人肺腺癌Anip973 细胞系细胞的增殖有显著抑制作用；(2)
水飞蓟宾作用Anip973 细胞48h 后，随着浓度的增加，倒置显微镜下可见细胞数目减少，胞体变小、变圆，到高浓度时出现较多的
死亡细胞；(3) 扫描电镜观察发现，随着水飞蓟宾作用浓度的增加，Anip973 细胞中出现增多的凋亡细胞，凋亡细胞表现出典型的
超微结构特征；(4) 流式细胞仪检测的结果发现，随着药物作用时间的延长，Anip973 细胞的G1 期细胞比例增多，S 期细胞明显减
少，G2 期细胞略有减少，并出现明显的凋亡峰。（5）水飞蓟宾作用后的Anip973 细胞出现明显的DNA Ladder 和PARP 降解增加
等凋亡特征；（6）水飞蓟宾作用后，Anip973 细胞中的凋亡相关蛋白Bax 表达增加、caspase-3 和caspase-9 酶活性增加，而Bcl-2 表
达降低。结论：水飞蓟宾在体外有抑制人肺腺癌细胞Anip973 的增殖作用，并通过激活线粒体依赖的caspase 凋亡通路，诱导其凋
亡。 |
| 英文摘要: |
| Objective: To investigate the molecular mechanism of Sliybinin-induced apoptosis of Lung Cancer Cell Anip973.
Methods: The cancer cell apoptosis was detected by methyl thiazolyl tetrazolium (MTT) colorimetric assay, morphological observations
with inverted microscope and electron microscope, flow cytometry, DNA ladder analysis, expression analysis of PARP as well as the expression
and activity analysis of some apoptosis-related proteins including Bax, Bcl-2, caspase-3 and caspase-9. Results: (1) Sliybinin had
significant inhibiting effect on the cellular proliferation of Anip973 cells; (2) When treated by Sliybinin for 48 hours, with the increasing
of the concentrations, the number of Anip973 cells decreased, the cell body became smaller and more circular under light microscope,
and the number of dead cells escalated with an increased concentration of silymarin treatment. (3) More Anip973 cells presented apoptosis
and these cells appeared typical ultrastructural features with the increasing of Sliybinin concentration; (4) The proportion of Anip973
cells in G1 phase increased, and the number of cells in S phase decreased significantly, which reduced slightly in G2 phase and also presented
significant apoptotic peak with the prolongation of drug action; (5) The Anip973 cells treated with Sliybinin presented distinct
apoptotic features including DNA ladder, PARP degradation, etc; (6) In Anip973 cells treated with Sliybinin, the expression of Bax and
the enzyme activities of caspase-3 and caspase-9 increased, while the expression of Bcl-2 decreased. Conclusions: Sliybinin can inhibit
the proliferation of human lung adenocarcinoma cell line Anip973 and induce its apoptosis by activating the mitochondria-dependent caspase
cascade pathway. |
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