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[COX-2抑制剂塞来昔布对HL-60细胞增殖、凋亡的影响及其机制]

[Effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of HL-60 cells and its mechanism].

作者信息

Xie Xia, Li Jie, Wang Rui-Cang, Geng Rui-Li, Wang Su-Yun, Wang Chao, Zhao Xiao-Yun, Hao Hong-Ling

机构信息

Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.

Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China. E-mail:

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2014 Jun;22(3):707-11. doi: 10.7534/j.issn.1009-2137.2014.03.025.

Abstract

This study was aimed to investigate the effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of human acute myeloid leukemia cell line HL-60 and its mechanism. HL-60 cells were cultured with different concentrations of celecoxib for 24 h. Cell proliferation was analyzed by CCK-8 assay, cell apoptosis and cell cycle distribution were detected by flow cytometry. Cyclin D1, cyclin E1 and COX-2 mRNA expressions were determined by RT-PCR. The results showed that after the HL-60 cells were treated with different concentrations of celecoxib for 24 h, the cell growth was significantly inhibited in a dose-dependent manner(r = 0.955), IC50 was 63.037 µmol/L of celecoxib. Celecoxib could effectively induce apoptosis in HL-60 cells also in dose-dependent manner(r = 0.988), blocked the HL-60 cells in the G0/G1 phase. The expression of cyclin D1, cyclin E1 and COX-2 mRNA were downregulated. It is concluded that celecoxib can inhibit the proliferation of HL-60 cells in dose-dependent manner, celecoxib causes cell G0/G1 arrest and induces cell apoptosis possibly through down-regulation of the cyclin D1 and cyclin E1 expression, and down-regulation of COX-2 expression respectively.

摘要

本研究旨在探讨COX-2抑制剂塞来昔布对人急性髓系白血病细胞系HL-60增殖、凋亡的影响及其机制。用不同浓度的塞来昔布培养HL-60细胞24小时。采用CCK-8法分析细胞增殖,通过流式细胞术检测细胞凋亡和细胞周期分布。用RT-PCR法检测细胞周期蛋白D1、细胞周期蛋白E1和COX-2 mRNA的表达。结果显示,用不同浓度的塞来昔布处理HL-60细胞24小时后,细胞生长呈剂量依赖性显著抑制(r = 0.955),塞来昔布的IC50为63.0 μmol/L。塞来昔布也能以剂量依赖性方式有效诱导HL-60细胞凋亡(r = 0.988),使HL-60细胞阻滞于G0/G1期。细胞周期蛋白D1、细胞周期蛋白E1和COX-2 mRNA的表达下调。结论:塞来昔布能剂量依赖性抑制HL-60细胞增殖,塞来昔布可能分别通过下调细胞周期蛋白D1和细胞周期蛋白E1的表达以及下调COX-2的表达导致细胞G0/G1期阻滞并诱导细胞凋亡。

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