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环氧化酶-2 抑制剂联合依托泊苷对肺癌细胞增殖凋亡的影响[J]. 肿瘤防治研究, 2005, 32(11): 689-691. DOI: 10.3971/j.issn.1000-8578.3193
引用本文: 环氧化酶-2 抑制剂联合依托泊苷对肺癌细胞增殖凋亡的影响[J]. 肿瘤防治研究, 2005, 32(11): 689-691. DOI: 10.3971/j.issn.1000-8578.3193
The Effects of Nimesul ide Combined with Etoposide on Lung Cancer Cell Proliferation and Apoptosis[J]. Cancer Research on Prevention and Treatment, 2005, 32(11): 689-691. DOI: 10.3971/j.issn.1000-8578.3193
Citation: The Effects of Nimesul ide Combined with Etoposide on Lung Cancer Cell Proliferation and Apoptosis[J]. Cancer Research on Prevention and Treatment, 2005, 32(11): 689-691. DOI: 10.3971/j.issn.1000-8578.3193

环氧化酶-2 抑制剂联合依托泊苷对肺癌细胞增殖凋亡的影响

The Effects of Nimesul ide Combined with Etoposide on Lung Cancer Cell Proliferation and Apoptosis

  • 摘要: 目的 探讨环氧化酶-2(COX-2)抑制剂尼米舒利(NIM)与化疗药依托泊苷(VP-16)联用对肺癌细胞增殖和凋亡的影响。方法 培养人肺癌细胞A549:①NIM(25μmol/L)与VP-16(2~32μg/mL)联合,MTT试验观察干预48h后细胞增殖变化及增殖抑制率;②分为对照组、NIM组(25μmol/L)、VP-16组(8μg/mL)和NIM+VP.16组,观察12h、24h及48h后A549细胞生长情况,描记生长曲线;流式细胞术检测干预48h后细胞凋亡率。结果 ①VP-16能抑制肺癌A549细胞的增殖,且呈量一效关系(r=-0.908,P〈0.01),NIM与VP-16联用后,抑增殖作用增强,二者有相加或协同作用;②NIM及VP-16均可抑制A549细胞的生长,诱导凋亡,二者联用后作用增强。结论 NIM与VP-16联用可增强对肺癌细胞增殖的抑制和凋亡的诱导,二者具有协同抗肿瘤作用。

     

    Abstract: Objective  To investigate the effect s of cyclooxygenase-2 selective inhibitor nimesulide (NIM) combined with etoposide (VP-16) on cell proliferation and apoptosis in human lung cancer. Methods  Human lung cancer A549 cells were incubated and the studies were done as follows : ①NIM (25μmol/ L) combined with VP-16 (2~32μg/ mL) coincubated with A549 cells for 48h, the cell proliferation status and proliferation inhibition rate were detected by MTT reduction assay. ②The cells were divided into control group, NIM (25μmol/ L ) group, VP-16 (8μg/ mL ) group and NIM + VP-16 group . The cells growth activity was observed by growth curve as cells coincubated for 12h, 24h, 48h, and the cell apoptosis rate was analyzed by flow cytomet ry. Results  ①VP-16 could inhibit A549 cells proliferation in a concent ration dependent pattern, which was enhanced as combined with NIM. NIM and VP-16 acted in a synergistic or additive pattern. ②NIM and VP-16 could induce A549 cells apoptosis effectively and the antitumor effects were augmented as they combined. Conclusion  NIM combined with VP-16 can enhance the effects of growth inhibition and apoptosis induction and they play a synergistic anti-tumor effect in lung cancer cell.

     

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