期刊文献+

γ-干扰素对肝纤维化大鼠肝Fas、Fas-L表达的影响 预览 被引量:1

Expression of Fas and Fas-L proteins in rat liver fibrosis model and the role of IFN-γ
在线阅读 下载PDF
收藏 分享 导出
摘要 目的:研究Fas、Fas-L蛋白在四氯化碳(CCl4)诱导肝纤维化模型大鼠肝组织中的表达以及γ-干扰素(IFN-γ)对其表达的影响.方法:用CCl4诱导制作大鼠肝纤维化模型,使用IFN-γ(20 mu·kg-1·d-1,肌肉注射)对该模型肝纤维化大鼠治疗12周,设正常对照组和模型对照组,用免疫组织化学法(EnVition法)检测各组大鼠肝组织Fas、Fas-L的表达情况.结果:Fas和Fas-L在正常对照组大鼠肝细胞质表达极低,在模型对照组大鼠肝组织主要表达在纤维间隔、肝窦中,表达的量均明显高于正常对照组(P<0.01).IFN-γ治疗组大鼠肝组织Fas和Fas-L的表达低于模型对照组(P<0.05~P<0.01).结论:肝纤维化时Fas和Fas-L表达加强,IFN-γ对肝纤维化大鼠肝组织Fas和Fas-L表达有明显的抑制作用. Objective:To study the expression of Fas and Fas-L proteins in rat liver fibrosis model and the role of IFN-γ.Methods:Liver fibrosis was successfully induced in rats by subcutaneous injection of carbon tetrachloride(CCl4).The rats were divided into fibrosis model group and IFN-γ treatment group(20 mu·kg-1·d-1,intramuscular injection for 12 weeks)and the group of rats without treatment was used as normal control.Fas and Fas-L proteins of the three groups were detected by immunohistochemistry.Results:Fas and Fas-L proteins were scarcely detected in the plasma of hepatocytes in the normal control,but they cound be found in the fibrous septae and hepatic sinusoid in fibrosis model rats(P<0.01).Compared with that in fibrosis models,the expression of Fas and Fas-L protein was significantly lower in rats treated with IFN-γ(P<0.05-P<0.01).Conclusions:The expression of Fas and Fas-L proteins is increased in rat liver fibrosis model.IFN-γ can inhibit the expression of Fas and Fas-L.
作者 俞小忠 陶君 蔡卫民 黄龚 朱辰 刘荣华 YU Xiao-zhong  TAO Jun  CAI Wei-min  HUANG Gong  ZHU Chen  LIU Rong-hua 
出处 《蚌埠医学院学报》 CAS 2007年第6期 643-645,封3,共4页 Journal of Bengbu Medical College
关键词 肝疾病 肝纤维化 Γ-干扰素 四氯化碳 FAS蛋白 FAS-L蛋白 liver diseases liver fibrosis IFN-γ carbon tetrachloride Fas albumen Fas-L albumen
  • 相关文献

参考文献6

二级参考文献28

  • 1[1]Brenner DA. Therapeutic strategy for liver fibrosis. J Gastroenterol Hepatol 1999; 14(Suppl. ): A279-A280 被引量:1
  • 2[2]Wu CH. Fibrodynamics-elucidation of the mechanisms and sites of liver fihrogenesis. World J Gastroenterol 1999; 5:388-390 被引量:1
  • 3[3]Liu CH, Hu YY, Wang XL, Liu P, Xu LM. Effect of salvianolic acid-A on NIH/3T3 fibroblast proliferation, collagen synthesis and gene expression. World J Gastroenterol 2000; 6:361-364 被引量:1
  • 4[4]Friedman SL. The cellular basis of hepatic fibrosis. Mechanisms and treatment strategies. N Engl J Med 1993; 328:1828-1835 被引量:1
  • 5[5]Liu SR, GuHD, LiDG, LuHM. A comparative study of fat storing cells and hepatocytes in collagen synthesis and collagen gene expression. Xin Xiaohuabingxue Zazhi 1997; 5:761-762 被引量:1
  • 6[6]Gu SW, Luo KX, Zhtang L, Wu AH, He HT, Weng JY. Relationship between ductile proliferation and liver fibrosis of chronic liver disease.Shijie Huaren Xiaohua Zazhi 1999; 7:845-847 被引量:1
  • 7[7]Yan JC, Ma Y, Chen WB, Shun XH. Dynamic observation on liver fibrosis and cirrhosis of hepatitis B. Huaren Xiaohua Zazhi 1998;6:699-702 被引量:1
  • 8[8]Wang Y, Gao Y, Huang YQ, Yu JL, Fang SG. Gelatinase A proenzyme expression in the process of experimental liver fibrosis. Shijie Huaren Xiaohua Zazhi 2000; 8:165-167 被引量:1
  • 9[9]Lu LG, Zeng MD, Li JQ, Qiu DK, Hua J, Fan ZP. Expression of intercellular adhesion molecular-1 by activated hepatic stellate cells.Huaren Xiaohua Zazhi 1998; 6:567-569 被引量:1
  • 10[10]Wang X, Chen YX, Xu CF, Zhao GN, Huang YX, Wang QL.Relationship between tumor necrosis factor-αand liver fibrosis. World J Gastroenterol 1998; 4:18 被引量:1

共引文献12536

同被引文献40

  • 1Shigeki Tsukada, Christopher J, Richard A. Mechanisms of liver fibro- sis[J]. Clinica Chimica Aeta, 2006, 364(4):3-60. 被引量:1
  • 2Davern TJ. Molecular therapeutics of liver disease[J]. Clinical in Liver Disease, 2001, 5(2): 381-414. 被引量:1
  • 3KatoR, KamiyaS, UekiM, et al. The fibronectin-derived antiadhesive peptide suppress the myofibroblastic conversion of rat hepatic stellat- ecells[J]. Ceil Resear- ch, 2001, 265:54-63. 被引量:1
  • 4Fort J, Oberti F, Pilette C, et al. Antifibrotic and hemodynamic effects of the early and chronic administration of octreotide in two models of liver fibrosis in rats[J]. Hepatology, 1998,28(6):1525-1531. 被引量:1
  • 5ROBERT G. BENNETT.Relaxin and its role in the development and treatment of fibrosis[J]. Translational Research, 2009, 154(3): 1-6. 被引量:1
  • 6Bennett RG, Kharbanda KK, Tuma DJ. Inhibition of markers of hepatic stellate cell activation by the hormone relaxin [J]. Bioche- mistry Pharmacology, 2003,66(7):867-874. 被引量:1
  • 7Bennett RG, Heimann DG, Tuma DJ. Retaxin reduces fibrosis in models of progressive and established hepatic fibrosis[J].Atmals NY Academic Science, 2009, 1160(1): 348-349. 被引量:1
  • 8Yoshitaka Nabeshima, Susumu Tazuma, Keishi Kanno, et al. Anti-fib- rogenic function of angiotansin II type 2 receptor in CC14-induced li- ver fibrosis [J]. Biochemical and Biophysical Research Communicati- ons, 2006, 346(3): 658-664. 被引量:1
  • 9Xu Li, Ying Meng, Pingsheng Wu, et al. Angiotensin Ⅱand Aldoste- rone stimulat- ing NF-KB and AP-1 activation in hepatic fibrosis of rat[J]. Regulatory Peptides 2007, 138 (1): 15-25. 被引量:1
  • 10Yamashita, T, Tokutomi, Y, Matsuba, S, et al. Olmesartan prevents c- ardiovascular injury and hepatic steatosis in obesity and diabetes, ac- companied by apoptosis signal regulating kinase-1 inhibition[J]. Hyp- ertension, 2008, 52(6):573-580. 被引量:1

引证文献1

二级引证文献1

投稿分析
职称考试

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 意见反馈