大鼠移植物血管病变模型的建立和研究

发布时间：2018-05-20 15:42

本文选题：动物模型 + 移植物血管病变　；参考：《复旦大学》2009年硕士论文

【摘要】： 第一部分大鼠移植物血管病变模型的建立目的:建立大鼠同种异体移植物血管病变模型以探讨其发病机制及进行干预研究。方法:将48只Wistar系和SD系大鼠分为两组:即同基因移植组(Wistar→Wistar)和异基因移植组(Wistar→SD)各24只。取供体胸降主动脉移植入受体腹主动脉,建立大鼠同种异体胸腹主动脉移植模型,分别在光镜和电镜下观察术后5、14、28天移植动脉病理改变,并用计算机图像分析系统分析血管管腔面积、内膜及中膜面积的变化。结果:移植术后28天,异基因移植组移植动脉出现显著的内膜增厚。典型的病理改变包括以增殖的平滑肌细胞及细胞外基质为主要成分的新生内膜形成以及内外膜炎症细胞浸润。而同基因移植组移植动脉与移植术前相比,未见明显差异。结论:用大鼠胸腹主动脉移植方法复制移植物血管病变模型是可行的,其病理改变类似于人类移植物血管病变的病变特点。此模型可用于移植物血管病变发病机制和防治措施的进一步研究。第二部分血管平滑肌细胞在移植物动脉硬化中的作用目的:观察移植物动脉硬化病变过程中血管平滑肌细胞增殖和凋亡的变化,探讨血管平滑肌细胞在移植物血管病变的作用。方法:Wistar大鼠18只,SD大鼠6只,按供、受鼠基因不同分为2组(每组6对):同基因移植组(Wistar→Wistar)和异基因移植组(Wistar→SD),施行胸腹主动脉移植术。术后28天取出大鼠移植动脉,分别在电镜和光镜下进行常规组织病理学观察及形态学测量,并用免疫组织化学方法测定增殖细胞核抗原(PCNA)及用TUNEL法检测血管壁平滑肌细胞的凋亡。结果:术后28天同基因移植组和异基因移植组移植动脉均可见平滑肌细胞增殖和凋亡,同基因移植组主要位于血管中层,而异基因移植组则位于新生内膜层。异基因移植组的内膜增生厚度、炎症细胞浸润程度及血管平滑肌细胞增殖指数和凋亡指数均明显高于同基因移植组(p＜0.05)。结论:血管平滑肌细胞参与移植性动脉硬化病理改变过程。血管平滑肌细胞病理性增殖速度大于其凋亡速度是移植动脉内膜增厚,管腔狭窄的主要原因。
[Abstract]:The first part: establishment of rat graft vascular lesion model Aim: to establish an allograft vascular lesion model in rats to investigate its pathogenesis and intervention. Methods: 48 Wistar and SD rats were divided into two groups: isogenic transplantation group (n = 24) and allogeneic transplantation group (n = 24). The donor descending aorta was transplanted into the recipient abdominal aorta to establish an allograft model of thoracic and abdominal aorta. The pathological changes of the transplanted artery were observed under light microscope and electron microscope at 5 ~ 1428 days postoperatively. The changes of vascular lumen area, intima and media area were analyzed by computer image analysis system. Results: 28 days after transplantation, there was significant intimal thickening in allogeneic transplantation group. Typical pathological changes include neointimal formation with proliferating smooth muscle cells and extracellular matrix as main components and infiltration of inflammatory cells inside and outside the membrane. However, there was no significant difference between the same gene transplantation group and before transplantation. Conclusion: it is feasible to establish graft vascular lesion model by using the method of thoracic and abdominal aortic transplantation in rats, and its pathological changes are similar to the pathological characteristics of human graft vascular disease. The model can be used to further study the pathogenesis and prevention of graft vascular disease. The role of vascular smooth muscle cells in graft arteriosclerosis Aim: to observe the proliferation and apoptosis of vascular smooth muscle cells in the process of graft arteriosclerosis and to explore the role of vascular smooth muscle cells in graft angiopathy. Methods Sixteen Sprague-Dawley rats (n = 18) were divided into two groups according to the donor genes. They were divided into 2 groups (6 pairs in each group: isogenic transplantation group: Wistar Wistar Wistar rats) and allogeneic transplantation group (n = 18). Thoracic and abdominal aortic transplantation was performed. The grafted arteries were taken out 28 days after operation, and the histopathology and morphology were observed under electron microscope and light microscope, respectively. Proliferating cell nuclear antigen (PCNA) and apoptosis of vascular smooth muscle cells (VSMCs) were detected by immunohistochemical method and TUNEL method. Results: smooth muscle cell proliferation and apoptosis were observed 28 days after operation in the allogeneic and allogeneic transplantation groups. The same gene transplantation group was mainly located in the middle vascular layer, while the allogeneic transplantation group was located in the neointimal layer. The thickness of intimal hyperplasia, the degree of inflammatory cell infiltration, the proliferation index and apoptosis index of vascular smooth muscle cells in allogeneic transplantation group were significantly higher than those in allogeneic transplantation group (P < 0.05). Conclusion: vascular smooth muscle cells are involved in the pathological changes of transplanted arteriosclerosis. The pathological proliferation rate of vascular smooth muscle cells was higher than that of apoptosis, which was the main cause of intimal thickening and stenosis of vascular smooth muscle cells.
【学位授予单位】：复旦大学
【学位级别】：硕士
【学位授予年份】：2009
【分类号】：R654.2;R-332

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