李靖, 程桂芳, 朱秀媛, 候琦. 白细胞介素类及白三烯类等炎性介质对肿瘤坏死因子α产生的影响J. 药学学报, 2000, 35(4): 261-264.
引用本文: 李靖, 程桂芳, 朱秀媛, 候琦. 白细胞介素类及白三烯类等炎性介质对肿瘤坏死因子α产生的影响J. 药学学报, 2000, 35(4): 261-264.
Li Jing Cheng Guifang Zhu Xiuyuan Hou Qi, . EFFECTS OF PRO-INFLAMMATORY CYTOKINES AND LEUKOTRIENS ON PRODUCTION OF TNFα FROM MURINE PERITONEAL MACROPHAGESJ. Acta Pharmaceutica Sinica, 2000, 35(4): 261-264.
Citation: Li Jing Cheng Guifang Zhu Xiuyuan Hou Qi, . EFFECTS OF PRO-INFLAMMATORY CYTOKINES AND LEUKOTRIENS ON PRODUCTION OF TNFα FROM MURINE PERITONEAL MACROPHAGESJ. Acta Pharmaceutica Sinica, 2000, 35(4): 261-264.

白细胞介素类及白三烯类等炎性介质对肿瘤坏死因子α产生的影响

EFFECTS OF PRO-INFLAMMATORY CYTOKINES AND LEUKOTRIENS ON PRODUCTION OF TNFα FROM MURINE PERITONEAL MACROPHAGES

  • 摘要: 目的:研究白细胞介素类及白三烯类等炎性介质对小鼠腹腔巨噬细胞生成及分泌肿瘤坏死因子α(TNFα)的影响。方法:用L929作为靶细胞的结晶紫染色法测定巨噬细胞培养上清液及胞溶部分TNFα的含量。结果:重组鼠白细胞介素-1β(rmIL-1β)和重组人白细胞介素-8(rhIL-8)均能促进巨噬细胞产生TNFα,其中rhIL-8有很好的剂量相关性,对巨噬细胞胞溶部分的TNFα无影响;重组人白细胞介素-6(rhIL-6),白三烯B4(LTB4),白三烯C4(LTC4)及白三烯D4(LTD4)均不能促进巨噬细胞生成及分泌TNFα。结论:rhIL-8和rmIL-1β能促进小鼠腹腔巨噬细胞生成TNFα。rhIL-6, LTB4, LTC4和LTD4对TNFα生成无影响。

     

    Abstract: AIM: To investigate production of TNFα from murine peritoneal macrophages stimulated with inflammatory mediator, such as IL-1, IL-6, IL-8, LTB4, LTC4 and LTD4. METHODS: L929 cytotoxicity was used to show the level of released and cell-associated TNFα in murine peritoneal macrophages measured by means of crystal violet staining assay. RESULTS: rhIL-8(40~4 000 U.mL-1) was shown to induce dose-dependent increase of released TNFα from murine macrophages. rmIL-1β(0.001~1μg.mL-1) was found to increase the level of released TNFα dose-independently, whereas rhIL-6(10~10 000 U.mL-1), LTB4(5.64×10-9~5.64×10-7mol.L-1), LTC4(1.73×10-9~1.73×10-7mol.L-1), LTD4(4.03×10-9~4.03×10-7mol.L-1) did not induce macrophages to produce TNFα. They all can not elevate cell-associated TNFα. CONCLUSION: The results suggest that rhIL-8 and rmIL-1 can induce production of TNFα from murine peritoneal macrophages, while rhIL-6, LTB4, LTC4 and LTD4 can not induce production of TNFα from murine peritoneal macrophages.

     

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