Glisson鞘综合征门静脉高压不可逆临界点的研究

发布时间：2018-10-29 15:46

【摘要】：目的:建立胆道梗阻的SD大鼠模型,探寻“Glisson鞘综合征”门静脉高压不可逆的临界点,探讨“Glisson鞘综合征”胆道压力、门静脉压力及病理变化情况,深入分析TGFβ1/Smad3信号通路在Glisson鞘综合征的变化情况。方法:1.结扎胆总管建立“Glisson鞘综合征”大鼠模型。2.测量胆总管、门静脉及肝功能变化情况。3.生物机能实验系统测量大鼠门静脉压力。4.HE、Masson染色确定肝纤维化程度,免疫组织化学图像分析观察肝脏α-平滑肌肌动蛋白(α-SMA)、TGF-β1、Smad3水平的变化及趋势。结果:1.成功建立“Glisson鞘综合征”动物模型。2.胆管结扎后胆总管及门静脉压力上升。早期解除胆道梗阻,门静脉压力可降至接近正常水平;建模时间达38天,解除胆道梗阻后,门静脉压力不能恢复正常,且病理检查发现假小叶的形成。3.免疫组化结果表明:TGF-β1与Smad3随着胆道梗阻时间延长表达增强。结论:1.在大鼠“Glisson鞘综合征”模型中,结扎胆总管后33-38天时间段内出现不可逆临界点,其标志为假小叶形成。2.TGFβ1/Smad3信号通路可能参与Glisson鞘综合征门静脉高压不可逆变化。
[Abstract]:Objective: to establish a SD rat model of biliary obstruction, to explore the irreversible critical point of portal hypertension in "Glisson sheath syndrome", and to explore the biliary pressure, portal vein pressure and pathological changes in "Glisson sheath syndrome". To investigate the changes of TGF 尾 1/Smad3 signaling pathway in Glisson sheath syndrome. Methods: 1. The rat model of Glisson sheath syndrome was established by ligation of common bile duct. 2. The changes of common bile duct, portal vein and liver function were measured. The portal vein pressure in rats was measured by biological function experiment system. 4. The degree of hepatic fibrosis was determined by HEMA Masson staining, and the changes and trends of 伪 -smooth muscle actin (伪-SMA), TGF- 尾 1) Smad3 levels in liver were observed by immunohistochemical image analysis. The result is 1: 1. Successful establishment of "Glisson sheath syndrome" animal model. 2. The pressure of common bile duct and portal vein increased after ligation of bile duct. The portal vein pressure could be reduced to the normal level at early stage, and the modeling time was up to 38 days. After relieving biliary obstruction, portal vein pressure could not return to normal, and pathological examination showed that pseudolobules were formed. Immunohistochemical results showed that the expression of TGF- 尾 1 and Smad3 increased with the prolongation of biliary obstruction time. Conclusion: 1. In the rat model of "Glisson sheath syndrome", the irreversible critical point appeared within 33-38 days after ligation of common bile duct, marked by pseudolobules formation. 2.TGF 尾 1/Smad3 signaling pathway may be involved in the irreversible changes of portal hypertension in Glisson sheath syndrome.
【学位授予单位】：湖南师范大学
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：R575.21

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