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前列腺素E_2对膀胱癌患者LAK细胞增殖及抗肿瘤细胞毒作用的影响 被引量:2

In vitro effects of prostaglandin E_2 on the proliferation of lymphokine activated killer cells and their cytotoxicity against bladder tumor cells in patients with bladder cancer
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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.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 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
关键词 LAK细胞 前列腺素E2 细胞毒 膀胱肿瘤 细胞增殖 Lymphokine activated killer cells Bladder cancer Proliferation Cytotoxicity Prostaglandin E_2
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  • 1陈大斌.非甾体类抗炎药抗肿瘤研究进展[J].川北医学院学报,2004,19(2):168-171. 被引量:2
  • 2徐振宇,许传亮,孙颖浩.RECK基因在前列腺组织中的表达及其与基质金属蛋白酶-9的关系[J].中华实验外科杂志,2005,22(9):1146-1146. 被引量:5
  • 3司文秀,杨继章.非甾体类抗炎药的抗癌作用及机制[J].中国药房,2007,18(19):1510-1512. 被引量:4
  • 4Kirkpatrick K, Ogunkolade W, Elkak A, et al. The mRNA expression of cyelooxygenase-2 (COX-2) and vascular endothelial growth faetor(VEGF) in human breast cancer [J]. Curr Med Res Opin ,2002,18(4) :237.
  • 5Andrzej S, Michael K.Inhibition of angiogenesis byNSA IDs: Mo2 lecular mechanisms and clinical imp lications[J].J Mol Med,2003, 81(1):27.
  • 6Kishi K. Preferential enhancement of tumor radioresponse hy a cyclooxygenase-2 inhibitor[J].Cancer IRes,2000,60:1326.
  • 7Chiu CH ,McEntee MF ,Whelan J.Sulindae causes rapid regression of preexisting tumors Mird+mice independent of prostagland in biosynthesis[J].Cancer Res, 1997,57(19):4267.
  • 8Liu JF,Jamieson GG, Drew PA, et al.Aspiria induces apoptosis in oesophageal cancer cells by inhibiting the pathway of NF - kappaB downst ream regulation of cyclooxygenase-2[J].A N Z J Surg,2005, 75(11):10111.
  • 9Kim WH,Yeo M ,Kim MS,et al.Role of caspase-3 in apoptosis of colon cancer induced by nonsteroidal anti-inflarmnatory dugs[J].I.nt JColorect Dis,2000,15(2):105.
  • 10Pique M, Barragan M, Dalmau M, et al.Aspirin induces apoptosis through mitochondrial cytochrome C release[J].FEBS letter,2000, 480(2/3):193.

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