中文摘要：

背景像胰岛素的生长因素绑定蛋白质相关的蛋白质(IGFBPrP1 ) 1 能激活肝的星形的房间并且在 vitro 增加细胞外的矩阵(ECM ) 。然而，在有肝的纤维变性的老鼠的 IGFBPrP1 的效果，和这些效果的机制，当前是未知的。我们在 thioacetamide (TAA ) 的这 study.Methods Intraperitoneal 注射瞄准这些问题到地址是为建立肝的纤维变性的一个老鼠模型的一个经典方法。用这个模型，我们管理了 anti-IGFBPrP1 抗体，再经由 intraperitoneal 注射。肝纤维变性的词法变化被观察与他和染色的马森。immunohistochemical 试金并且西方的弄污被用来在 IGFBPrP1 测量变化，光滑的肌肉肌动朊(在肝纸巾的 -SMA) 和 ECM，和转变生长 factor-1 (TGF-1 ) 和 Smad3 的表示。数据统计上用变化( ANOVA )的单程的分析被分析，为染色分析的马森显示出的团体之间的 differences.Results 的 SNK-q 测试与正常控制组相比，在 TAA5w 组的骨胶原纤维的内容是，这显著地增加了( P < 0.01 )，并且它显著地在 TAA5w/alGFBPrP1 组被减少与相比在 TAA5w 组( P < 0.01 )。肝的 IGFBPrP1 的表示， -SMA, TGF-1， Smad3，骨胶原我和 fibronectin (FN ) 在 TAA5w 组是显著地起来调整的(P < 0.01 ) 。Anti-IGFBPrP1 处理颠倒了这些变化(P < 0.01 ).Conclusions IGFBPrP1 在肝的纤维变性的发展起一个重要作用。Anti-IGFBPrP1 由压制肝的星形的房间的激活在老鼠阻止纤维变性，禁止 ECM 的主要部件的合成(也就是，骨胶原我和 FN ) 。为纤维变性的这抑制的机制与表明小径的 TGF-1/Smad3 被联系。

英文摘要：

Background Insulin-like growth factor binding protein-related protein 1 （IGFBPrP1） can activate hepatic stellate cells and increase extracellular matrix （ECM） in vitro. However, the effects of IGFBPrP1 in mice with hepatic fibrosis, and the mechanisms of these effects, are currently unknown. We aim to address these issues in this study. Methods Intraperitoneal injection of thioacetamide （TAA） is a classic method for establishing a mouse model of hepatic fibrosis. Using this model, we administered anti-IGFBPrP1 antibody, again via intraperitoneal injection. The morphological changes of liver fibrosis were observed with both HE and Masson stainning. The immunohistochemical assays and Western blotting were used to measure changes in IGFBPrP1, a-smooth muscle actin （a-SMA） and ECM in liver tissues, and the expression of transforming growth factor-β1 （TGF-β1） and Smad3. Data were statistically analyzed using one-way analysis of variance （ANOVA）, the SNK-q test for inter-group differences. Results The Masson staining analysis showed that compared with normal control group, content of collagen fiber in TAA5w group was significantly increased （P 〈0.01）, and it was significantly decreased in TAA5w/alGFBPrP1 group compared with in TAA5w group （P 〈0.01）. The expression of hepatic IGFBPrP1, a-SMA, TGF-β1, Smad3, collagen 1 and fibronectin （FN） was significantly up-regulated in the TAA5w group （P 〈0.01）. Anti-IGFBPrP1 treatment reversed these changes （P 〈0.01）. Conclusions IGFBPrP1 plays an important role in the development of hepatic fibrosis. Anti-IGFBPrP1 prevents fibrosis in mice by suppressing the activation of hepatic stellate cells, inhibiting the synthesis of major components of the ECM （namely, collagen I and FN）. The mechanism for this suppression of fibrosis is associated with the TGF-β1/Smad3 signaling pathways.