期刊文献+

小鼠机体炎症反应促进纤维肉瘤生长的作用

Inflammatory response promotes the growth of fibrosarcoma in the mice model
原文传递
导出
摘要 目的探讨小鼠机体炎症反应促进纤维肉瘤生长的作用及可能机制。方法 C57BL/6小鼠随机分为正常对照组(PBS组)、脂多糖组(LPS组)、纤维肉瘤组(PC组)、脂多糖+纤维肉瘤组(LC组)、脂多糖+纤维肉瘤+塞来昔布组(Cele组),PBS组小鼠腹腔注射PBS缓冲液,其余各组小鼠给以脂多糖(LPS)建立炎症模型,实验第5天处死LPS组、PBS组小鼠,其余组小鼠皮下接种纤维肉瘤细胞,同时Cele组小鼠给予塞来昔布,接种肿瘤第21天处死小鼠。比较各组小鼠的一般状况及肿瘤体积,处死小鼠后取肺组织观察外形改变及组织病理学特点,应用CD31染色比较PC组及LC组小鼠肿瘤的血管形态及微血管密度(MVD)。结果与PBS组相比,LPS组小鼠肺组织血管通透性增高,组织液渗出增多,肺泡腔内可见大量红细胞、炎症细胞;与PC组相比,LC组小鼠肿瘤生长速度快,肿瘤MVD增加,血管紊乱。结论炎症反应对纤维肉瘤的生长有促进作用,其机制可能与促进肿瘤血管生成有关,抗炎治疗可抑制纤维肉瘤的生长。 Objective To study the effects of inflammation on the growth of tumor in fibrosarcoma-bearing mice and the possible mechanism. Methods C57BL/6 mice were randomly divided into 5 groups: the normal control group ( PBS group), the lipopolysaccharide group ( LPS group), the fibrosarcoma group ( PC group), the LPS + fibrosarco- ma group (LC group), and the LPS + fibrosarcoma + celecoxib group (Cele group). PBS buffer was intraperitoneal- ly injected to the PBS group mice, and the remaining groups were given lipopolysaccharide (LPS) to establish the in- flammation model. The mice of the LPS and PBS groups were killed on the fifth day, and the rest were subcutaneously inoculated with fibrosarcoma cells. Meanwhile the Cele group mice were given celecoxib and the mice were sacrificed 21 days after the inoculation. The general conditions and tumor volumes of the mice were compared. Mice were sacri- riced, and the profile changes and the pathological characteristics of the lung tissues were studied. Tumor microvascular density and vessel phenotype of PC group and LC group mice were compared by CD31 staining. Results Compared with the PBS group, the lung vascular permeability and the tissue fluid exudation increased, and a large number of red blood cells and inflammatory cells were observed in the LPS group. Compared with the PC group, the tumors in the LC group grew faster, the microvascular density increased and the blood vessels were in disorder. Conclusion The inflam- matory response promotes the growth of fibrosarcoma possibly by the promotion of the tumor angiogenesis. Anti-inflam- matory treatment can inhibit the growth of fibrosarcoma.
出处 《山东大学学报(医学版)》 CAS 北大核心 2013年第1期7-11,共5页 Journal of Shandong University:Health Sciences
基金 国家自然科学基金(81272351) 山东省自然科学基金(2R2012HM020) 山东省科技发展计划(2012G0021826)
关键词 纤维肉瘤 炎症 血管生成 脂多糖 小鼠 Fibrosarcoma Inflammation Angiogenesis Lipopolysaccharide Mice
  • 相关文献

参考文献19

  • 1Eiro N, Vizoso F J. Inflammation and cancer[J]. World J Gastrointest Surg, 2012, 4(3) :62-72.
  • 2Mantovani A, Allavena P, Sica A, et al. Cancer-related inflammation [ J ]. Nature, 2008, 454 ( 7203 ) : 436 -..4 a..
  • 3Multhoff G, Molls M, Radons J. Chronic inflammation in cancer development [J]. Front Immunol, 2011, 2 : 98. Epub 2012 Jan 12.
  • 4Yang S Y, Yu H Y, Kryjier J E, et al. High VEGF with Rapid Growth and Early Metastasis in Mouse Osteosarcoma Model[ J]. Sarcoma, 2007, 2007:95628.
  • 5Cao R, Bjorndahl M A, Gallego M I, et al. Hepatocyte growth factor is a lymphangiogenic factor with an indirect mechanism of action [J]. Blood, 2006, 107 ( 9 ) : 3531- 3536.
  • 6Weidner N, Folkman J, Pozza F, et al. Tumor angiogenesis: a new significant and independent prognostic indicator in early-stage breast carcinoma [J]. J Natl Cancer Inst, 1992, 84(24) :1875-1887.
  • 7Harmey J H, Bucana C D, Lu W, et al. Lipopolysaccharide-induced metastatic growth is associated with increased angiogenesis, vascular permeability and tumor cell invasion[J]. Int J Cancer, 2002, 101(5) :415-422.
  • 8He Z, Zhu Y, Jiang H. Inhibiting toll-like receptor 4 signaling ameliorates pulmonary fibrosis during acute lung injury induced by lipopolysaccharide: an experimental study [J]. Respiratory Research, 2009, 10:126.
  • 9Le Bitoux M A, Stamenkovic I. Tumor-host interactions: the role of inflammationl J]. Histochem Cell Biol, 2008, 130(6) :1079-1090. Epub 2008 Oct 25.
  • 10Allavena P, Sica A, Garlanda C, et al. The Yin-Yang of tumor-associated macrophages in neoplastic progression and immune surveillance[ J ]. Immunol Rev, 2008, 222.155-161.

二级参考文献96

  • 1Kerbel R,Folkman J.Clinical translation of angiogenesis inhibitors[J].Nat Rev Cancer,2002,2(10):727.
  • 2Naldini A,Carraro F.Role of inflammatory mediators in angiogenesis[J].Curr Drug Targets Inflamm Allergy,2005,4(1):3.
  • 3Kundu JK,Surh YJ.Inflammation:Gearing the journey to cancer[J].Mutat Res,2008,659(1/2):15.
  • 4Sun B,Zhang S,Zhang D,et al.Doxycycline influences microcirculation patterns in B16 melanoma[J].Exp Biol Med,2007,232(10):1300.
  • 5Bergers G,Benjamin LE.Tumorigenesis and the angiogenic switch[J].Nat Rev Cancer,2003,3(6):401.
  • 6Folkman J.Tumor angiogenesis:therapeutic implications[J].N Engl J Med,1971,285(2):1182.
  • 7Lin WW,Karin M.A cytokine-mediated link between innate immunity,inflammation,and cancer[J].J Clin Invest,2007,117(5):1175.
  • 8Balkwill F, Mantovani A. Inflammation and cancer:back to Virchow? Lancet 2001; 357:539-45.
  • 9Coussens LM, Werb Z. Inflammation and cancer.Nature 2002; 420:860-7.
  • 10Hussain SP, Harris CC. Inflammation and cancer: an ancient link with novel potentials. Int J Cancer 2007; 121:2373-80.

共引文献26

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部