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rhIL-10对肿瘤坏死因子-α诱导的血管外膜成纤维细胞增殖的影响 被引量：1

Effects of recombinant human interleukin-10on tumor necorsis factor-α-induced adventitial fibroblast proliferation in vitro
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摘要 目的观察重组人白细胞介素-10(rhIL-10)对肿瘤坏死因子-α(TNF-α)诱导的成纤维细胞增殖的影响。方法体外培养NIH/3T3细胞,应用rhIL-10与TNF-α共同作用并设立对照进行比较,采用MTS/PES法确定NIH/3T3细胞的增殖状态。应用流式细胞仪测定细胞周期。结果TNF-α对NIH/3T3细胞增殖具有明显的刺激作用。rhIL-10单独应用对NIH/3T3细胞生长没有影响。在TNF-α刺激下,一定剂量的rhIL-10可抑制NIH/3T3细胞的增殖。rhIL-10可使TNF-α作用下的NIH/3T3细胞大部分处于G0/G1期。结论rhIL-10能明显抑制由TNF-α刺激的成纤维细胞增殖。 Objective To observe the effects of recombin an t human interleukin-10 (rhIL-10) on adventitial fibroblast prolifer-ation induce d by tumor necrosis factor-α(TNF-α)in vitro. Methods In this controlled stud y, NIH/3T3 cells cultured in vitro were treated with TNF-αand recombinant human interleukin-10 (rhIL-10), respectively, and the cell proliferation was deter-mi ned by non-radioactive MTS/PES assay. Cell cycle analysis was performed using fl ow cytomertry. Results Compared with the control cells, TNF-αsignificantly sti mulated NIH/3T3 cell proliferation, wherea. rhIL-10 had no such effect. With TNF -αstimulation, rhIL-10 at the dose as low as 1 ng/ml inhibited the proliferatio n of NIH/3T3 cells (P<0.05). The number of cells in G 0 /G 1 phase treated with both TNF-αand rhIL-10 was higher than those treated wit h TNF-αalone (P<0.05), as shown by flow cytometry. Conclusion rhIL-10 can sign ificantly inhibit the proliferation of adventitial fibroblasts induced by TNF-α in vitro.
作者 欧阳平 孟素荣 刘彦波 许顶立 赖文岩 彭立胜 徐安龙
机构地区 广州第一军医大学附属南方医院心血管内科 广州中山大学生命科学学院生物化学系
出处 《第一军医大学学报》 CSCD 北大核心 2004年第1期50-52,共3页 Journal of First Military Medical University
基金 广州市科委科技攻关项目(JB00000448165)~~
关键词 RHIL-10 肿瘤坏死因子-Α 血管外膜 成纤维细胞 重组人白细胞介素-10 细胞增殖 fibroblasts/drug effects interleukin-10 tumor necorsis fact or cell growth
分类号 R543 [医药卫生—心血管疾病]
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参考文献9

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同被引文献16

  • 1张彬,欧阳平,陈烨,赖文岩,谢晋国,许顶立.肿瘤坏死因子α对人脐静脉内皮样细胞增殖及syndecan-4蛋白表达的影响[J].南方医科大学学报,2007,27(4):496-498. 被引量：4
  • 2张彬,刘振华,欧阳平,陈烨,赖文岩,许顶立.肿瘤坏死因子α对大鼠平滑肌细胞增殖及syndecan-4蛋白表达的影响[J].中华神经医学杂志,2007,6(7):657-659. 被引量：8
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  • 4KOO B K,JUNG Y S,SHIN J,et al.Structural basis of syndecan -4 phosphorylation as a molecular switch to regulate signaling[J].Mol Biol,2006,355(4):651-663.
  • 5DEEPA S S,YAMADA S,ZAKO M,et al.Chandroitin sulfate chains on syndecan-1 and syndecan-4 from normal murine mammary gland epithelial cells are structurally and functionally distinct and cooperate with heparan sulfate chains to bind growth factors.A novel function to control binding of midkine,pleiotrophin,and basic fibroblast growth factor[J].Bial Chem,2004,279(36):37 368-37 376.
  • 6TKACHENKO E,ELFENBEIN A,TIRZIU D,et al.syndecan4 clustering induces cell migration in a PDZ-dependent manner[J].Circ Bes,2006,98(11):1398-1404.
  • 7WANG L C,FUSTER M,SRIRAMARAO P,et al.Endothe]ial heparan sulfate deficiency impairs L-selectin-and chemokinemediated meutrophil trafficking during inflammatory responses[J].Nature Immuno,2005,6(9):902-910.
  • 8LOPES C C,TOMA L,PINHAL M A S,et al.EJ-ras oncogene transfectian of endothelial cells upregulates the expression of syndecan-4 and downrngulates heparan sulfate sulfotransferases and epimerase[J].Biochimie,2006,88(1):1493-1504.
  • 9RAUCH B H,MILLETTE E,KENAGY R D,et al.syndecan-4 is required for thrombin-induced migration and proliferation in human vascular smooth muscle cells[J].Biol Chem,2005,280(17):17507-17511.
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第一军医大学学报
2004年 第1期

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