發(fā)布時(shí)間：2018-05-20 15:42

  本文選題：動(dòng)物模型 + 移植物血管病變�。� 參考：《復(fù)旦大學(xué)》2009年碩士論文

【摘要】： 第一部分大鼠移植物血管病變模型的建立 目的:建立大鼠同種異體移植物血管病變模型以探討其發(fā)病機(jī)制及進(jìn)行干預(yù)研究。 方法:將48只Wistar系和SD系大鼠分為兩組:即同基因移植組(Wistar→Wistar)和異基因移植組(Wistar→SD)各24只。取供體胸降主動(dòng)脈移植入受體腹主動(dòng)脈,建立大鼠同種異體胸腹主動(dòng)脈移植模型,分別在光鏡和電鏡下觀察術(shù)后5、14、28天移植動(dòng)脈病理改變,并用計(jì)算機(jī)圖像分析系統(tǒng)分析血管管腔面積、內(nèi)膜及中膜面積的變化。 結(jié)果:移植術(shù)后28天,異基因移植組移植動(dòng)脈出現(xiàn)顯著的內(nèi)膜增厚。典型的病理改變包括以增殖的平滑肌細(xì)胞及細(xì)胞外基質(zhì)為主要成分的新生內(nèi)膜形成以及內(nèi)外膜炎癥細(xì)胞浸潤(rùn)。而同基因移植組移植動(dòng)脈與移植術(shù)前相比,未見明顯差異。 結(jié)論:用大鼠胸腹主動(dòng)脈移植方法復(fù)制移植物血管病變模型是可行的,其病理改變類似于人類移植物血管病變的病變特點(diǎn)。此模型可用于移植物血管病變發(fā)病機(jī)制和防治措施的進(jìn)一步研究。 第二部分血管平滑肌細(xì)胞在移植物動(dòng)脈硬化中的作用 目的:觀察移植物動(dòng)脈硬化病變過程中血管平滑肌細(xì)胞增殖和凋亡的變化,探討血管平滑肌細(xì)胞在移植物血管病變的作用。 方法:Wistar大鼠18只,SD大鼠6只,按供、受鼠基因不同分為2組(每組6對(duì)):同基因移植組(Wistar→Wistar)和異基因移植組(Wistar→SD),施行胸腹主動(dòng)脈移植術(shù)。術(shù)后28天取出大鼠移植動(dòng)脈,分別在電鏡和光鏡下進(jìn)行常規(guī)組織病理學(xué)觀察及形態(tài)學(xué)測(cè)量,并用免疫組織化學(xué)方法測(cè)定增殖細(xì)胞核抗原(PCNA)及用TUNEL法檢測(cè)血管壁平滑肌細(xì)胞的凋亡。 結(jié)果:術(shù)后28天同基因移植組和異基因移植組移植動(dòng)脈均可見平滑肌細(xì)胞增殖和凋亡,同基因移植組主要位于血管中層,而異基因移植組則位于新生內(nèi)膜層。異基因移植組的內(nèi)膜增生厚度、炎癥細(xì)胞浸潤(rùn)程度及血管平滑肌細(xì)胞增殖指數(shù)和凋亡指數(shù)均明顯高于同基因移植組(p＜0.05)。 結(jié)論:血管平滑肌細(xì)胞參與移植性動(dòng)脈硬化病理改變過程。血管平滑肌細(xì)胞病理性增殖速度大于其凋亡速度是移植動(dòng)脈內(nèi)膜增厚,管腔狹窄的主要原因。
[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.
【學(xué)位授予單位】：復(fù)旦大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2009
【分類號(hào)】：R654.2;R-332

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本文編號(hào)：1915262