前列腺素E2或吲哚美辛对膀胱癌患者淋巴因子激活杀伤细胞增殖的影响及其对膀胱肿瘤细胞的细胞毒性

Wang Zhiping , Chen Yirong , Zheng Rongliang , Qin Dashan , Chen Xuehong , Wang Yiqiu , Liu Guodong
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引用次数: 8

摘要

目的:探讨白细胞介素-2 (IL-2)联合前列腺素E2 (PGE2)或吲哚美辛(IM)对膀胱癌患者膀胱肿瘤细胞增殖及淋巴因子活化杀伤(LAK)细胞溶解的影响。方法:采用细胞计数法测定不同浓度PGE2和IM对LAK细胞增殖的影响。以患者膀胱癌BIU-87、EJ和膀胱肿瘤细胞(BTC)为靶细胞,采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑(MTT)法检测LAK细胞的细胞毒性。此外,用放射免疫法(RIA)测定了21例膀胱癌患者和20例健康供者的膀胱癌细胞或外周血单个核细胞(PBMC)条件培养基样品和血浆中的PGE2。结果:PGE2 (0.05 ~ 5 ng/mL)对IL-2诱导的LAK细胞增殖有抑制作用,且呈浓度依赖性。在一定浓度的IM (100 ~ 400 ng/mL)处理48 ~ 96 h后,LAK细胞的生长明显增强。IM (200 ng/mL)预处理LAK细胞对BIU-87、EJ细胞和BTC的细胞毒性显著增强。BIU-87细胞条件培养基中PGE2含量高于PBMC条件培养基。结论:这些研究表明,PBMC和膀胱癌细胞产生的PGE2可抑制IL-2诱导的膀胱癌患者LAK细胞增殖。这种抑制作用可被IM所克服,可能用于膀胱癌的免疫治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
In Vitro Effects of Prostaglandin E2 or Indomethacin on the Proliferation of Lymphokine-Activated Killer Cells and their Cytotoxicity against Bladder Tumor Cells in Patients with Bladder Cancer

Purpose: To investigate the combined effects of interleukin-2 (IL-2) with either prostaglandin E2 (PGE2) or indomethacin (IM) on the proliferation and cytolysis of bladder tumor cells by lymphokine-activated killer (LAK) cells in patients with bladder cancer.

Methods: LAK cell proliferation was assayed in the presence of various concentrations of either PGE2 or IM by cell counting. Bladder cancer cell lines BIU-87, EJ and bladder tumor cells (BTC) from the patients were cultured as target cells, and the cytotoxicity of LAK cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In addition, PGE2 in samples of conditioned medium from bladder cancer cells or peripheral blood mononuclear cells (PBMC) as well as plasma from 21 patients with bladder cancer and 20 healthy donors were determined by radioimmunoassay (RIA).

Results: The proliferation of LAK cells induced by IL-2 was inhibited by PGE2 (0.05 to 5 ng/mL) in concentration-dependent manner. The enhanced growth of LAK cells was observed at certain concentrations of IM (100–400 ng/mL) from 48 to 96 h. Pretreatment of LAK cells with IM (200 ng/mL) significantly enhanced cytotoxicity against BIU-87, EJ cells, or BTC. More PGE2 was present in conditioned medium from BIU-87 cells than in the conditioned medium from PBMC.

Conclusions: These studies indicate that LAK cell proliferation induced by IL-2 in patients with bladder cancer is inhibited by PGE2 produced by PBMC and bladder cancer cells. This inhibition can be overcome by IM, which may be of use in immunotherapy of bladder cancer.

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