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DcR3在预防博莱霉素大鼠模型发生肺纤维化中的作用 被引量:2

Preliminary study of DcR3 prevention bleomycin pulmonary fibrosis in rats
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摘要 目的探讨DcR3在预防博莱霉素大鼠模型发生肺纤维化中的作用。方法采用博莱霉素复制肺纤维化动物模型。分为正常对照组、博莱霉素组、博莱霉素+DcR3组,给药时间2 w,各组分别于2、4、6、8 w处死大鼠6只,收集肺泡灌洗液的细胞和上清检测细胞因子含量。左肺组织冻存留作羟脯氨酸检测;右肺组织固定用作组织染色。结果博莱霉素+DcR3组肺泡炎的程度表现为逐渐减轻的过程,炎症程度均低于BL组(P<0.05);BL+DcR3组肺纤维化程度无明显加重趋势,与对照组比较差异显著(P<0.05),与BL组比较有显著性差异(P<0.01)。结论 DcR3的早期应用,可减轻博莱霉素大鼠模型肺的的局部炎症,可能在一定程度上达到预防肺纤维化形成的目的。 Objective To investigate the role of DcR 3 in preventing bleomycin rat model of pulmonary fibrosis .Methods The ble-omycin animal model of pulmonary fibrosis was established .The animal models were divided into normal control , bleomycin, bleomycin +DcR3 groups.The alveolar lavage fluid cells were cultured and supernatant , and the levels of cytokines were detected .Results The degree of alveolitis was reduced in Bleomycin+DcR3 group, which was lower than that of BL group (P<0.05);and the degree of lung fibrosis was not significantly increased trend in Bleomycin +DcR3 group,which had significant difference compared with that of BL and control groups (P<0.05, P<0.01).Conclusions DcR3 early application could reduce lung local inflammation in bleomycin rat model , achieve the pur-pose of prevention of pulmonary fibrosis in some extent .
出处 《中国老年学杂志》 CAS CSCD 北大核心 2014年第9期2462-2465,共4页 Chinese Journal of Gerontology
基金 国家自然科学基金项目(30370617)
关键词 DCR3 炎症 肺纤维化 DcR3 Inflammation Pulmonary fibrosis
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参考文献6

  • 1Masayasu Takahashi,Yasushi Miura,Shinya Hayashi,Koji Tateishi,Koji Fukuda,Masahiro Kurosaka.DcR3-TL1A signalling inhibits cytokine-induced proliferation of rheumatoidsynovial fibroblasts[J].International Journal of Molecular Medicine.2011(3) 被引量:1
  • 2郏博,杨洋,齐欣萌,王春田,王宏茂,杜闯,王祥,马忠森.诱骗受体3对肺纤维化动物模型早期的作用[J].细胞与分子免疫学杂志,2010,26(6):602-603. 被引量:4
  • 3Chenyang Zhan,Yury Patskovsky,Qingrong Yan,Zhenhong Li,Udupi Ramagopal,Huiyong Cheng,Michael Brenowitz,Xiao Hui,Stanley G. Nathenson,Steven C. Almo.Decoy Strategies: The Structure of TL1A:DcR3 Complex[J].Structure.2011(2) 被引量:1
  • 4S. Hayashi,T. Nishiyama,Y. Miura,T. Fujishiro,N. Kanzaki,S. Hashimoto,T. Matsumoto,M. Kurosaka,R. Kuroda.DcR3 induces cell proliferation through MAPK signaling in chondrocytes of osteoarthritis[J].Osteoarthritis and Cartilage.2011(7) 被引量:1
  • 5Koji Fukuda,Yasushi Miura,Toshihisa Maeda,Masayasu Takahashi,Shinya Hayashi,Masahiro Kurosaka.Decoy receptor 3 regulates the expression of various genes in rheumatoidarthritis synovial fibroblasts[J].International Journal of Molecular Medicine.2013(4) 被引量:1
  • 6O. Eickmeier,L. v. d. Boom,F. Schreiner,M. J. Lentze,D. NGampolo,R. Schubert,S. Zielen,S. Schmitt-Grohé,Pham My-Chan Dang.Transforming Growth Factor β 1 Genotypes in Relation to TGF β 1, Interleukin-8, and Tumor Necrosis Factor Alpha in Induced Sputum and Blood in Cystic Fibrosis[J].Mediators of Inflammation.2013 被引量:1

二级参考文献6

  • 1吴艳峰,杨俊玲,马忠森,董春玲,秦彦国.DcR_3基因与特发性肺纤维化肺功能的相关性研究[J].中国老年学杂志,2004,24(10):894-895. 被引量:2
  • 2Antoniou KM, Alexandrakis MG. Cytokine network in the pathogenesis of idionpathic pulmonary fibrosis [ J ]. Sarcoidosis Vasc Diffuse Lung Dis, 2005, 22(2) : 91 -95. 被引量:1
  • 3Pitti RM, Marsters SA, Lawrence DA, et al. Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer[ J]. Nature, 1998, 396(6712): 699-703. 被引量:1
  • 4Mary Philip A, Donald A, Rowley B, et al. Inflammation as a tumor promoter in cancer induction [J].Semi Cancer Biol, 2004, 214 (14) : 433 -439. 被引量:1
  • 5Szczeklik J, Trojan J, Kopinski P, et al. Apoptosis of bronchoalveolar lavage lymphocytes ( L-BAL ) in pneumoconiosis [ J ]. Przegl Lek, 2004, 61(4): 235-240. 被引量:1
  • 6Petersen BL, Rengtved P, Bank MI, et al. High expression of markers of apoptosis in Langerhans cell histiocytosis [ J ]. Histopathology, 2003, 42(2) : 186 - 193. 被引量:1

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