前列腺素H合成酶2（PGHS-2）在血管损伤后内膜增生中的作用

发布时间：2018-06-06 12:23

本文选题：小鼠模型 + 狭窄　；参考：《南昌大学》2011年硕士论文

【摘要】：背景目的：前列腺素H合成酶(PGHS),也称环氧合酶(COX),是前列腺素类物质合成的关键酶,它在动脉粥样硬化、血管成形术后狭窄等血管炎性疾病的发展中扮演着重要的作用。虽然COX-2选择性抑制剂有增加心脏病发作和中风的危险,但是我们对它在介入治疗后血管重塑中的作用知之甚少。本实验利用COX-2 K0、COX-1COX-2(COX-1基因插入C0X-2位点)转基因小鼠的动脉损伤模型,揭示COX-2来源的前列腺素表达对血管损伤后内膜增生狭窄的影响。方法结果：本实验通过建立股动脉血管损伤小鼠动物模型,利用免疫荧光和HE染色判断小鼠股动脉损伤模型是否建立成功,采用HE染色法、Envision免疫组织化学法、利用image pro plus软件分析小鼠内膜和中膜面积比(I/M ratio),描述COX-2 K0、COX-1＞COX-2转基因小鼠和野生型小鼠股动脉损伤后四周的特征。VSMC标记物(α-actin)免疫组化结果显示在所有损伤小鼠中,损伤血管内膜几乎全由血管平滑肌组成。COX-2 K0小鼠的股动脉病变中的巨噬细胞和中性粒细胞浸润明显少于COX-1＞COX-2(P0.05)和WT小鼠(P＜0.01)。COX-2 K0小鼠同COX-1COX-2(4.534±1.274,PK0.05)和WT对照组小鼠(4.534±1.274,P＜0.05)相比内膜／中膜比明显降低。上述结果表明,COX-2缺失可以防止血管平滑肌细胞反应性增殖。结论： COX-2来源前列腺素参与损伤引起的动脉重构。这些结果表明,阻断COX-2的下游信号可能提供一种方法防止血管成形术后再狭窄的动脉阻塞。
[Abstract]:Background objectives: Prostaglandin H synthase (PGHSN), also known as cyclooxygenase, is a key enzyme in the synthesis of prostaglandins, which plays an important role in the development of vasculitis such as atherosclerosis, angioplasty and stenosis. Although selective inhibitors of COX-2 may increase the risk of heart attack and stroke, little is known about its role in vascular remodeling after interventional therapy. In this study, the arterial injury model of transgenic mice with COX-2 K0 COX-1COX-1 gene inserted into C0X-2 site was used to reveal the effect of prostaglandin expression derived from COX-2 on intimal hyperplasia and stenosis after vascular injury. Method results: In this experiment, the animal model of femoral artery vascular injury was established, and the success of the model was determined by immunofluorescence and HE staining, and the envision immunohistochemical method was used to determine the success of the model. The image pro plus software was used to analyze the ratio of intima and medial area of COX-2 K0 COX-1 > COX-2 transgenic mice and wild-type mice after femoral artery injury. The immunohistochemical results of 伪 -actinin showed that the expression of 伪 -actinin was found in all the injured mice. The invasion of macrophages and neutrophils in femoral artery lesions of injured vascular intima was almost entirely composed of vascular smooth muscle. The infiltration of macrophages and neutrophils in femoral artery lesions of the injured vascular intima was significantly less than that of COX-1 > COX-2 (P0.05) and WT mice (P < 0.01).COX-2 K0 vs COX-1COX-2(4.534 卤1.274PK0.05) and WT control mice (4.534 卤1.274P < 0.05). These results suggest that COX-2 deficiency can prevent reactive proliferation of vascular smooth muscle cells. Conclusion: Prostaglandins derived from COX-2 are involved in arterial remodeling caused by injury. These results suggest that blocking downstream signals of COX-2 may provide a way to prevent restenosis after angioplasty.
【学位授予单位】：南昌大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R363

【参考文献】