摘要/Abstract
摘要： 目的·探索肝硬化门静脉高压症（portal hypertension，PHT）大鼠的肠系膜上动脉（superior mesenteric artery，SMA）重构现象。方法·将大鼠分为正常对照组（8只）、CCl4吸入8周PHT组（8只）和CCl4吸入12周PHT组（10只）。成模后，对所有大鼠行血流动力学参数测定。取该3组大鼠的肝脏组织制备石蜡切片后，分别行苏木精-伊红染色（hematoxylin and eosin staining，H-E staining，H-E染色）、马松（Masson）染色和天狼星红（Sirius Red）染色。取3组大鼠的SMA组织制备冰冻切片后行H-E染色，定量分析其血管直径、血管壁厚度和血管面积。免疫组织化学法行钙调蛋白检测，免疫荧光法检测弹性蛋白、cleaved caspase-3蛋白（凋亡信号）和Ki-67蛋白（增殖信号）的表达，同时采用蛋白质印迹法对保存于液氮中的SMA的钙调蛋白和弹性蛋白进行检测。结果·与正常对照组相比，肝硬化PHT 8周组和12周组大鼠的门静脉压力升高、平均动脉压下降（均P＜0.05），即模型构建成功。与正常对照组相比，肝硬化PHT 12周组大鼠SMA血管壁厚度和面积减少，SMA中钙调蛋白、弹性蛋白表达减少，SMA的平滑肌细胞中凋亡信号增加（均P＜0.05）。结论·肝硬化PHT的SMA存在血管重构变薄现象，且相关收缩结构蛋白如钙调蛋白、弹性蛋白急剧减少，平滑肌层凋亡增多，受损严重。
关键词: 门静脉高压症, 动脉重构, 肝硬化
Abstract:
Objective · To investigate the remodeling of superior mesenteric artery (SMA) in cirrhotic portal hypertension (PHT) rats. Methods · The rats were divided into normal group (n=8), PHT group with CCl4 inhalation for 8 weeks (n=8) and PHT group with CCl4 inhalation for 12 weeks (n=10). After the model was established, hemodynamic parameters of all the rats were measured. The liver tissues of the three groups were prepared for paraffin section, and then stained with hematoxylin and eosin staining (H-E staining), Masson staining and Sirius Red staining, respectively. After frozen sections of SMA tissues were prepared, H-E staining was performed to quantitatively analyze the lumen diameter, wall thickness and area of SMA. Caldesmon expression was detected by immunohistochemistry. The expression of elastin, cleaved caspase-3 protein (apoptotic signal) and Ki-67 protein (proliferation signal) were detected by immunofluorescence, and caldesmon and elastin of SMA in liquid nitrogen were detected by Western blotting. Results · Compared with the normal control group, portal pressure increased and mean arterial pressure decreased in PHT group with CCl4 inhalation for 8 and 12 weeks (all P<0.05), which meant the PHT model was successfully established. Compared with the normal group, the thickness and area of SMA vessel wall and the expression of caldesmon and elastin in SMA were decreased, and the apoptosis signal of SMA smooth muscle cells was increased in PHT group with CCl4 inhalation for 12 weeks (all P<0.05). Conclusion · The vascular remodeling of SMA in PHT with cirrhosis is thinning, and the expression of related contractile structural proteins such as caldesmon and elastin decrease sharply, while apoptosis signal of smooth muscle layer increases and related damage is serious.
Key words: portal hypertension (PHT), arterial remodeling, liver cirrhosis
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