目的 构建小鼠胆总管结扎(BDL)及四氯化碳(CCl4)诱导的两种门静脉高压症(PHT)模型.方法24只C57BL/6小鼠,随机分成4组(BDL组及相应对照组,CCl4诱导组及相应对照组),每组6只.BDL及CCl4诱导法构建PHT小鼠模型后,经门静脉主干穿刺测取门静脉压,并通过血清谷氨酸转氨酶(ALT)及天冬氨酸转氨酶(AST)水平检测,肝脏切片苏木精-伊红(HE)及天狼星红染色,平滑肌肌动蛋白(SMA)免疫组化检查分别对模型肝功能、肝纤维化及肝星状细胞激活情况进行评价.结果两种建模方法均使小鼠门静脉压上升,导组上升更为显著.两模型组小鼠与相应对照组相比,均呈现严重肝功能损伤、肝纤维化及肝星状细胞激活.结论BDL及CCl4诱导方法均能成功构建PHT小鼠模型,其门静脉压、血清学生化指标及肝脏病理学改变均符合PHT特点.%Objective To establish two types of portal hypertension (PHT) models in mice by using bile duct ligation (BDL) method and carbon tetrachloride (CCl4) induction technique respectively. Methods A total of 24 C57BL/6 mice were randomly and equally divided into the following four groups with 6 mice in each group: group BDL, control group of BDL, group CCl4, and control group of CCI4. After the establishment of PHT, the main portal vein was punctured in all experimental mice to measure the portal vein pressure, and blood sampling was collected to test serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Using hematoxylin eosin (HE) and sirius red staining the liver tissues were pathologically examined. Immunohistochemical study of alpha smooth muscle actin (SMA) was adopted to evaluate the liver function, hepatic fibrosis and hepatic stellate cell activation status. Results Both modeling methods could make the portal vein pressure increased in experimental mice. The increasing of portal vein pressure in group CCl4 was more obvious. Compared with their corresponding control groups, the degree of liver damage, hepatic fibrosis and hepatic stellate cell activation in group BDL and group CCl4 were more serious. Conclusion Both BDL method and CCl4 induction technique can successfully establish the mouse model of PHT. All the portal venous pressure, the serum biochemical indices and the changes of liver pathology of the mouse model are well in line with the characteristics of PHT in human. (J Intervent Radiol, 2018, 27:242-246)
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