中文摘要：

目的探讨血管紧张素（1-7）（Ang（1—7））对胆管结扎所致肝纤维化大鼠肝窦血管生成的抑制作用及相应的分子机制。方法将18只Wistar雄性大鼠随机分为假手术（SHAM）组，胆总管结扎（BDL）组和Ang（1—7）治疗组。假手术组：行开腹术再关腹，在腹腔埋注射泵，以25μg·kg-1·h-1。的速度持续注射等渗盐水；BDL组：开腹结扎胆总管建立肝纤维化模型，同时在腹腔埋注射泵，以25μg·kg-1·h-2的速度持续注射等渗盐水；Ang（1—7）治疗组：BDL建立肝纤维化模型，同时在腹腔埋注射泵，以25μg·kg-1·h-1的速度持续注射Ang（1—7）。4周后宰杀动物，取肝组织，行苏木素一伊红染色，进行肝纤维化评分；Masson胶原染色，测定胶原的表达；利用免疫组织化学，免疫印迹（Westernblot），组织免疫荧光检测血管生成的标志：血管性血友病因子（vwF），血管内皮细胞生长因子A（vEGFA），血小板一内皮细胞黏附分子CD31的表达。根据资料不同采用One-wayANOVA检验、LSD法、Welch法、Durmett’s T3法、t检验或相关性分析。结果研究结果显示：在BDL组中，与SHAM组相比，肝纤维化评分（4．83±0．75对比0．00±0．00，Ｐ=0．000）、胶原面积（87．27±5．33对比0．98±0．11，P=0．000）、免疫组织化学检测vWF的表达（灰度值3．11±0．3对比1．00±0．07，Ｐ=0．000）、VEGFA的表达（灰度值8．38±1．64对比1．00±0．08，Ｐ=0．003）、CD31的表达（灰度值3．05±0．44对比1．00±0．12，P=0．000），Westernblot检测vWF的表达（灰度值0．380±0．008对比0．270±0．007，P=0．000）、VEGFA的表达（灰度值0．270±0．005对比0．120±0．002，P=0．007）、CD31的表达（灰度值0．350±0．008对比0．060±0。004，P=0．000）均明显增高，差异有统计学意义护值均〈0．01）；免疫荧光检测BDL组肝组织vWF、VEGFA、CD31阳性表达细胞较SHAM组明显

英文摘要：

Objective To explore the inhibitory effect of angiotensin （1-7） on hepatic sinusoid angiogenesis using a rat model of hepatic fibrosis. Methods Eighteen male Wistar rats were randomly divided into three equal groups for sham operation （untreated/uninduced control group）, bile duct ligation （BDL） （untreated model group）, or BDL with angiotensin （1-7） treatment （treated model group）. Histological analysis was used to assess the liver fibrosis score, by hematoxylin-eosin staining, and the level of fibrosis, by Masson＇s trichrome staining. Immunohistochemistry, western blotting, and immunofluorescence were used to assess the expression of the angiogenesis markers vWF, VEGFA, and CD31. Results Compared with the untreated/uninduced control group, the untreated BDL model group showed remarkably higher fibrosis score, area of the type I collagen expression, and expression levels of vWF, VEGFA, and CD31. However, the angiotensin （1-7）-treatment protected against the BLD-related changes, as evidenced by decreased robustness and down-regulation of the corresponding indicators. Moreover, the expression level of VEGFA was highly correlated to the expression level of vWF （r= 0.956, P = 0.000）. Conclusion BDL-induced hepatic fibrosis is accompanied by significant increases in angiogenesis-related factors, but angiotensin （1-7） treatment may inhibit hepatic sinusoid angiogenesis during the liver fibrosis process.