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作 者:史葆光[1] 王志平[1] 陈一戎[1] 秦大山[1] 陈雪红[2] 王亦秋[2]
机构地区:[1]兰州医学院第二附属医院泌尿外科研究所,730030 [2]兰州医学院第二附属医院同位素室
出 处:《中华实验外科杂志》1999年第1期18-19,共2页Chinese Journal of Experimental Surgery
基 金:甘肃省自然科学基金!ZQ-96-12
摘 要:目的探讨前列腺素E_2(PGE_2)在膀胱癌患者淋巴因子激活的杀伤细胞(LAK)增殖及细胞毒的作用。方法LAK细胞培养于含不同浓度的PGE_2;的培养基中,并用细胞计数法测定其细胞增殖率,以BIU87、EJ及患者自体肿瘤细胞为靶细胞,用MTT法测定LAK细胞对膀胱癌细胞的细胞毒作用。结果0.05~5μg/L。PGE_2对LAK细胞的增殖呈浓度依赖性抑制。PGE_2LAK细胞对膀胱癌细胞的杀伤则影响不明显。膀胱癌细胞系BIU87的条件培养基的PGE_2含量明显高于PBMC的条件培养基。结论膀胱癌患者由IL-2诱导的LAK增殖可被由PBMC和膀胱癌细胞产生的PGE_2所抑制。Objective To investigate the combined effects of interleukin-2 (IL-2) with prostaglandin E_2 (PGE_2 ) on the proliferation and cytolysis of bladder tumor cells by lymphokine activated killer (LAK) cells in patients with bladder cancer. Method LAK cell proliferation was assayed in the presence of various concentrations of PGE_2 by cell counting. Bladder cancer cell lines BIU-87, EJ and bladder tumor cells from the patients were cultured as target cells, and cytotoxicity of LAK cells were determined by 3 - (4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Result The proliferation of LAK cells induced by IL-2 was inhibited by PGE_2 (0. 05 to 5 ng/ml) in a dose dependent manner. The level of PGE_2 in conditioned media from BIU-87 was significantly higher than that in the conditioned media from PBMC. Conclusion LAK cell proliferation induced by IL-2 in patients with bladder cancer is inhibited by PGE_2 produced by PBMC and bladder cancer cells.
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