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IL-4对TNF-α和IL-1β诱导的肺癌细胞分泌C3及B因子的研究

Effect of interleukin-4 on the secretion of complement 3 and factor B induced by tumor necrosis factor-α or interleukin-1β in lung cancer cell line A549

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【作者】 赵玉霞王志宇李光于润江

【Author】 ZHAO Yu-xia~(1),WANG Zhi-yu~(1),LI Guang~(1),YU Run-jiang~(2)(1.Department of Radiotherapy,The First Affiliated Hospital,China Medical University,Shenyang 110001,China;2.Institute of Respiratory Diseases)

【机构】 中国医科大学附属第一医院放射肿瘤科中国医科大学附属第一医院呼吸疾病研究所 辽宁沈阳110001辽宁沈阳110001

【摘要】 目的:探讨IL-4对TNF-α和IL-1β诱导的肺癌细胞分泌C3及B因子的影响。方法:分别用ELISA及RT-PCR法检测C3、B因子蛋白及mRNA表达。结果:TNF-α和IL-1β增强A549细胞分泌C3及B因子分别是对照组的6.4、7.5倍和6.0、8.9倍;IL-4增强A549细胞分泌C3是对照组的4.8倍,对B因子的分泌没有影响,但剂量依赖性上调TNF-α和IL-1β诱导的A549细胞分泌C3及下调TNF-α和IL-1β诱导的A549细胞分泌B因子。C3及B因子的mRNA表达与蛋白水平的结果相一致。结论:IL-4、TNF-α和IL-1β相互作用调节A549细胞分泌C3及B因子。

【Abstract】 Objective: To explore the effect of interleukin-4(IL-4) on the secretions of complement 3(C3) and factor B induced by tumor necrosis factor-α(TNF-α) or interleukin-1β(IL-1β) in lung cancer cells.Methods: Both protein and mRNA expressions of C3 and factor B in lung cancer cell line A549 were determined by enzyme-linked immunosorbent assay,Western blotting,and reverse transcriptase polymerase chain reaction. Results: The secretions of C3 and factor B induced by TNF-α were 6.4 and 7.5 times more than those in the control group,and the secretions induced by IL-1β were 6.0 and 8.9 times more than those in the control group. IL-4 increased the secretion of C3,which was 4.8 times more than that in the control group,but it had no effect on the secretion of factor B.IL-4 increased the secretion of C3 induced by TNF-α or IL-1β but decreased the secretion of factor B induced by TNF-α or IL-1β in a dose-dependent manner.The expression of mRNA was consistent with that of protein.Conclusion: IL-4 regulates the secretions of C3 and factor B induced by TNF-α or IL-1β in lung cancer cell line A549.

【关键词】 细胞因子补体肺癌
【Key words】 cytokinescomplementlung cancer
【基金】 辽宁省博士启动基金资助项目(201102048)
  • 【文献出处】 中国医科大学学报 ,Journal of China Medical University , 编辑部邮箱 ,2006年01期
  • 【分类号】R734.2
  • 【被引频次】1
  • 【下载频次】95
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