癌变·畸变·突变 ›› 2016, Vol. 28 ›› Issue (4): 255-261.doi: 10.3969/j.issn.1004-616x.2016.04.002

• 论著 • 上一篇    下一篇

塞来昔布对T细胞淋巴瘤细胞增殖及侵袭功能的影响

马鸣1, 杨兴肖2, 王雪晓3, 刘丽华3, 赵连梅3, 杜彦艳1, 单保恩3   

  1. 1. 河北医科大学第四医院检验科, 河北 石家庄 050011;
    2. 河北医科大学第四医院感染管理科, 河北 石家庄 050011;
    3. 河北医科大学第四医院科研中心, 河北 石家庄 050011
  • 收稿日期:2015-11-17 修回日期:2016-02-25 出版日期:2016-07-31 发布日期:2016-07-31
  • 通讯作者: 单保恩,E-mail:shanbaoen@163.com E-mail:shanbaoen@163.com
  • 作者简介:马鸣,E-mail:maming19830419@163.com
  • 基金资助:
    河北省卫生厅指令性课题(20150305)

Effects of celecoxib on proliferation and invasion of T cell lymphoma

MA Ming1, YANG Xingxiao2, WANG Xuexiao3, LIU Lihua3, ZHAO Lianmei3, DU Yanyan1, SHAN Baoen3   

  1. 1. Clinical Laboratory of the Fourth Hospital of Hebei Medical University, Shijiazhuang 050011;
    2. Department of Infection Management of the Fourth Hospital of Hebei Medical University, Shijiazhuang 050011;
    3. Research Center of the Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei, China
  • Received:2015-11-17 Revised:2016-02-25 Online:2016-07-31 Published:2016-07-31

摘要: 目的:研究塞来昔布对T细胞淋巴瘤细胞增殖、化疗敏感性及侵袭能力的影响,并探讨其作用机制。方法:分别用不同浓度(0、20、40及80μmol/L)塞来昔布处理T细胞淋巴瘤Jurkat和Hut78细胞系24、48和72 h后,采用MTT法检测Jurkat和Hut78细胞的增殖活性。再用40μmol/L塞来昔布处理Jurkat和Hut78细胞48 h后,采用MTT法检测其对化疗药物敏感性的影响;流式细胞术检测塞来昔布对Jurkat和Hut78细胞凋亡水平的影响;Transwell小室检测塞来昔布致Jurkat和Hut78细胞侵袭能力的变化;实时荧光定量PCR (qPCR)及Western blot技术分别从mRNA及蛋白水平检测塞来昔布对Jurkat和Hut78细胞系P38、P65、Bcl-2、Bax、MDR1、MMP2及MMP9表达水平的影响。结果:与对照组比较,20~80μmol/L塞来昔布作用于Jurkat和Hut78细胞不同时间后,细胞增殖活性均受到明显抑制(P<0.05)。40μmol/L塞来昔布对化疗药物的敏感性明显增强(P<0.05),且凋亡水平明显增加(P<0.01);与40μmol/L塞来昔布共培养的Jurkat和Hut78细胞,其穿透Transwell小室的能力明显下降(P<0.01),且P38及Bax蛋白的表达水平均明显增加(P均<0.01),而P65、MDR1、Bcl-2、MMP2及MMP9表达水平均明显降低(P均<0.01)。结论:塞来昔布对T表型淋巴瘤细胞增殖和侵袭能力具有明显抑制作用,提示其在T细胞淋巴瘤的临床治疗中具有应用前景。

关键词: 塞来昔布, T细胞淋巴瘤, 增殖, 侵袭

Abstract: OBJECTIVE: To investigate the effect of celecoxib on proliferation, chemotherapy sensitivity and invasion of T cell lymphoma. METHODS: Jurkat and Hut78 cells were treated with celecoxib for 24, 48 and 72 h, and their proliferation activity and chemotherapy sensitivity were detected using the MTT method. In addition, apoptotic rates of the treated cells were analyzed using flow cytometry. Transwell chamber was used to investigate the invasion of cells which were treated with celecoxib for 48 h. Expression of P38, P65, Bcl-2, Bax, MDR1, MMP2 and MMP9 in treated cells were investigated using quantitative real-time PCR (qPCR) and Western blot. RESULTS: After treatment with celecoxib, growth of Jurkat and Hut78 cells was inhibited in a dose-and time-dependent manner, and their chemotherapy sensitivity was elevated. Consequently, the apoptotic rates of the treated cells were also higher than the control. The number of treated cells that passed through Transwell chamber was significantly less than control (P<0.01). The qPCR and Western blot analyses showed that expression of P65, Bax, MDR1, Bcl-2, MMP2 and MMP9 were all down-regulated, whereas P38 and Bax were up-regulated in the treated cells compared with control(P<0.05). CONCLUSION: Celecoxib has inhibitory effect on proliferation and invasion of T cell lymphoma. Therefore, it may have a broad prospect for clinical treatment of T cell lymphoma.

Key words: celecoxib, T cell lymphoma, proliferation, invasion

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