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细胞因子对血吸虫病肝纤维化形成的影响(综述) 被引量:1

The effect of cellular factors on hepatic fibrosis of schistosomiasis japonica
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摘要 目的:探讨细胞因子对血吸虫病肝纤维化形成的影响。方法:查阅近10年国内外相关文献,并对文献进行分析、综述。结果:肝纤维化是血吸虫病的一个重要病理改变,细胞因子在血吸虫病性肝纤维化的发生发展过程中起着重作用,其中促肝纤维化的细胞因子是转化生长因子β1(TGF-β1)、血小板衍生生长因子(PDGF)、肿瘤坏死因子-α(TNF-α)、白介素(IL-1、IL-2、IL-4、IL-5、IL-6、IL-8、IL-13)、碱性成纤维细胞生长因子(bFGF)等,抗肝纤维化细胞因子是干扰素-γ(IFN-γ)、IL-10、IL-12、IL-18等。结论:深入研究细胞因子在肝纤维化形成机制中的作用有重要意义。 Objective To probe into the effect of cellular factors on hepatic fibrosis of schistosomiasis japonica.Methods To cousult the related domestic and foreign articles of last ten years for analyzing and summarizing. Results Hepatic fibrosis is one of the most important pathological feature in schistosomiasis japonica,and during the course of hepatic fibrosis in schistosomiasis japonica the cellular factors play major roles. Among the cellular factors ,some drive the hepatic fibrosis in schistosomiasis japonica,such as transforming growth factor- β 1,platelet- derived growth factor,tumor necrosis factor- α ,interleulin- 1, interleulin- 2,interleulin- 4,interleulin- 5,interleulin- 6,interleulin- 8,interleulin- 13, basic fibroblast growth factor and so on;some inhibit the hepatic fibrosis in schistosomiasis japonica,such as interferon- γ , interleulin- 10, interleulin- 12, interleulin- 18 and so on.Conclusion It is important to go on with further study on the effect of cellular factors on hepatic fibrosis of schistosomiasis japonica.
作者 吴义春 吴强
出处 《安徽卫生职业技术学院学报》 2003年第6期44-47,共4页 Journal of Anhui Health Vocational & Technical College
关键词 肝纤维化 血吸虫病 细胞因子 细胞外基质 ECM hepatic fibrosis schistosomiasis cytokine
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  • 1Holmes WE, Lee J, Kuang WJ, et al. Structure and functional ex- press ion of a human interleukin-8 recepto[J]. Science, 1991, 253 (5025): 1278-1280.
  • 2Murphy PM, Tiffany Hk Cloning of a complimentary DNA encodinga functional human interleukin-8 receptor [J]. Science, 1991, 253 (5025): 1280-1283.
  • 3Li F, Gordon JR. IL-8 (3-73) KllR is a high affinity agonist of the neutrophil CXCR1 and CXCR2[J]. Biochem Biophys Res Commun, 2001, 286(3): 595-600.
  • 4Li F, Zhang X, Gordon JR. CXCL8(3-73)KllR/G31P antagonizes ligand binding to the neutmphil CXCRI and CXCR2 receptors and cellular responses to CXCL8/IL-8[J]. Biochem Biophys Res Commun, 2002, 293 (3): 939-944.
  • 5Li F, Zhang X, Mizzi C, et al. CXCL8 (3-73)KllR/G31P antago- nizes the neutrophil chemoat tractants present in pasteurellosis and mastitislesions and abrogates neutrophil influx into intradermal endotoxin challenge sites in vivo [J]. Vet Immunol Immunopathol, 2002, 90(1-2): 65-77.
  • 6Gordon JR, Li F, Zhang X, et al. The combined CXCRI/CXCR2 antagonist CXCL8 (3-73)K 11 PriG31P blocks neutrophil infiltra- tion, pyrexia, and pulmonary vascular pat hology in endotoxemic animals[J]. J Leukocyte Biol, 2005, 78(6): 1265-1272.
  • 7Zhao X, Li F, Town JR, et al. Humanized forms of the CXCR1/ CXCR2 antagonist, bovine CXCL8 (3-73)K11R/G31P, effectively block ELR-CXC chemokine activity and airway endotoxemia pathology [ J ]. Int Immunopharmacol, 2007, 7 ( 13): 1723-1731.
  • 8Koch AE, Polverini PJ, Kunkel SL, et al. Interleukin-8 as a macrophage derived mediator of angiogenesis[J]. Science, 1992, 258(5089): 1798-1801.
  • 9Kishi H, Mikawa T, Seto M, et al. Stable transfectants of smooth muscle cell line lacking the expression of myosin light chain ki- nase and their characterization with respect to the actomyosin system[J]. J Biol Chem, 2000, 275(2): 1414-1420.
  • 10Zhang Y, Yu G, Xiang Y, et al. Bm-TFF2, a toad trefoil factor, promotes cell migration, survival and wound healing [J]. Biochem Biophys Res Commun, 2010, 398(3): 559-564.

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