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卵巢切除对四氯化碳诱导大鼠肝纤维化形成的影响 被引量:4

Impacts of ovariectomy on CCl_4-induced hepatic fibrosis of rats
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摘要 为探讨卵巢切除对CCl4 诱导大鼠肝纤维化形成的影响 ,采用CCl4 诱导雌性大鼠肝纤维化动物模型 ,观察卵巢切除及雌激素替代治疗 (苯甲酸雌二醇 1mg kg)对肝脏胶原沉积和I、Ⅲ型胶原蛋白表达的影响 ,并分别检测血清学标志及肝脏组织学等变化。结果显示CCl4 模型组大鼠肝脏发生典型的肝纤维化改变 ,卵巢切除组的肝脏胶原沉积更为明显 ,肝脏表达I、Ⅲ型胶原及血清肝纤维化指标也明显高于CCl4 摸型组 (P <0 0 5 ) ,而雌激素干预及替代治疗则可抑制肝纤维化的形成。表明卵巢切除加速CCl4 诱导大鼠肝纤维化的形成 ,其发生可能与卵巢分泌的雌激素对肝纤维化的抑制作用有关。 To study the effects of ovariectomy on CCl 4 induced hepatic fibrosis in rats and to investigate the suppressive effects of estrogen on liver fibrosis. Liver fibrosis was induced in ovariectomized rats by CCl 4 administration and then treated with benzoic estradiol(1mg/kg) twice a week. The expression of type I and Ⅲ collagen, the hepatic collagen synthesis and other indicators were studied. Results demonstrated that in CCl 4 group with typical liver fibrosis. ovariectomy aggravated hepatic collagen content, increased AST, ALT, hyaluronic acid(HA) and type IV collagen(CIV) in serum and enhanced expression of type I and Ⅲ collagen significantly in the fibrotic rats. Estradiol replacement therapy had an opposite effect. It was showed that ovariectomy aggravated CCl 4 induced hepatic fibrosis in rats. The mechanism may be explained by antifibrogenic effect of estrogen in liver.
出处 《基础医学与临床》 CSCD 北大核心 2003年第5期551-555,共5页 Basic and Clinical Medicine
基金 西安交通大学博士学位论文基金 (2 0 0 10 13)
关键词 卵巢切除 四氯化碳 大鼠 肝纤维化 肝脏组织学 雌激素 hepatic fibrosis ovariectomy estrogen
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  • 1Shigeo Sugano,Takashi Kawafune,Tugio Okajima,Kunihiko Ishii,Manabu Watanabe,Naoko Takamura. Chronic Splanchnic Hemodynamic Effects of Spironolactone with Unrestricted Sodium Diet in Patients with Compensated Cirrhosis[J] 1998,Digestive Diseases and Sciences(4):893~897

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  • 1王小众.肝纤维化的发病机制及抗纤维化研究进展[J].中西医结合肝病杂志,2001,11(S1):35-38. 被引量:3
  • 2Issa R, Williams E, Trim N, et al. Apoptosis of hepatic stellate cells:involvement in resolution of biliary fibrosis and regulation by soluble growth factors[J].Gut,2001,48:548-557.
  • 3Friedman SL. Cellular source of collagen and regulation of collagen production in liver[J] . Dis, 1990,10( 1 ) :20 - 29.
  • 4Basile DP. The transforming growth factor beta system in kidney disease and repair: recent progress and future directions [ J ]. Curr Opin Nephrol Hypertens, 1999,8:21 - 30.
  • 5Greenwel P, Schwartz M, Rossas M, et al. Characterization of fat-storing cell lines derived from normal and CCl4-cirrhotic livers[J]. Lab Invest, 1991,65:644 - 653.
  • 6Liu C, Gaca MD, Swenson ES , et al. Smads 2 and 3 are differentially activated by transforming growth factor-beta (TGF-beta) in quiescent and activated hepatic stellate cells.Constitutive nuclear loculization of Smads in activated cells is TGF-betaindependent[J].J Biol Chem,2003,278(13):11721-11728.
  • 7Razzaque MS, Taquchi T. Cellular and molecular events leading to renal tubulointerstitial fibrosis. Med Electron Microsc, 2002,35: 68-80.
  • 8Liu YH. Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. J Am Soc Nephrol, 2004,15: 1-12.
  • 9Jinde K, Nikolie-Paterson DJ, Huang XR, et al. Tubular phenotypic change in progressive tubulointerstitial fibrosis in human glomerulonephritis. Am J Kidney Dis,2001,38: 761-763.
  • 10Kodo S, Kagami S, Urushihara M, et al. Transforming growth factor-betal stimulates collagen matrix remodeling through increased adhesive and contractive potential by human renal fibroblasts. Biochim Biophys Acta, 2004,23: 1693; 2: 91-100.

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