P物质及血管活性肠肽在声带息肉中的表达

发布时间：2018-05-29 21:22

本文选题：声带息肉P物质 + 血管活性肠肽　；参考：《昆明医学院》2010年硕士论文

【摘要】： 【中文摘要】目的：检测P物质(Substance P)、血管活性肠肽(Vasoactive Intestinal Polypeptide,VIP)在声带息肉中的表达,了解神经肽对声带息肉患者发病的影响,进一步探讨声带息肉的发病机理。方法：选取经病理诊断确诊,且排除其他声带病变的声带息肉患者标本40例为实验组。取正常声带组织标本20例为对照组。所有标本经HE染色后,进行MaxVision~(TM)免疫组织化学染色,并行计算机图像定量分析。结果：在正常声带中,SP和VIP的表达较弱,而在声带息肉组织中的上皮细胞、炎性细胞、血管内皮细胞、腺体细胞、成纤维细胞表达较强。声带息肉组SP阳性单位均值(40.4833±5.83513)高于正常声带组(34.1300±5.56434)，，有统计学差异(p0.05)；声带息肉组VIP阳性单位均值(47.5144±6.98540)高于正常声带组(24.2522±8.22501),也有统计学差异(p0.01)。用声带息肉中SP和VIP阳性单位均值做散点图,两变量之间不存在线性趋势,说明二者没有相关性。结论：在反复的声带损伤后,声带组织中的SP与VIP分泌增多,生物学作用为：(1)SP既可直接作用于血管内皮细胞上的SP特异性受体引起内皮依赖性舒血管效应,也可通过刺激肥大细胞释放组胺而间接作用于血管引起血管扩张,血浆外渗,进而声带局部充血水肿。VIP同样具有强烈的血管扩张作用,并可能增加血管内皮生长因子的表达,继而更加引起组织水肿。同时SP与VIP促进血管扩张,可以增加息肉的局部血供,促进息肉的不断长大。(2)SP与VIP可诱导炎症介质的释放,共同作用导致慢性炎症,引起炎性细胞浸润,血管内皮基底膜受损,外周血管通透性增加、血浆蛋白渗出,使一些本不易通过基底膜的血管内物质进入血管外,导致声带粘膜固有层组织水肿、扩张、静水压升高,从而破坏了作用于上皮下基底膜内外的原有的压力平衡,加速了声带息肉的形成,这也是SP及VIP参与炎症反应的理论依据、神经源性炎症的特点。(3)SP与VIP可能在腺体分泌增加、囊性扩张中起到重要作用。(4)SP可促进成纤维细胞的增生,并加强IL-1所致的成纤维细胞的增生反应,导致玻璃样变性等,固有层结缔组织排列紊乱,层状结构消失,息肉形成。
[Abstract]:Objective: to detect the expression of substance P substance (substance P), vasoactive Intestinal polypeptide (Vasoactive Intestinal polypeptide) in vocal cord polyps, to understand the effect of neuropeptides on the pathogenesis of vocal cord polyps, and to explore the pathogenesis of vocal cord polyps. Methods: 40 patients with vocal cord polyps diagnosed by pathological diagnosis and excluded from other vocal cord lesions were selected as experimental group. 20 normal vocal cord specimens were taken as control group. All the specimens were stained by HE and stained by MaxVisionTM immunohistochemical staining, and the quantitative analysis of computer images was performed. Results: the expression of SP and VIP was weak in normal vocal cords, but strong in epithelial cells, inflammatory cells, vascular endothelial cells, glandular cells and fibroblasts in vocal cord polyps. The mean value of SP positive unit in vocal cord polyp group (40.4833 卤5.83513) was higher than that in normal vocal cord group (34.1300 卤5.56434), and the mean value of VIP positive unit in vocal cord polyp group was 47.5144 卤6.98540, which was higher than that in normal vocal cord polyp group (24.2522 卤8.22501), and the difference was also significant (p 0.01). Using SP and VIP positive unit mean in vocal cord polyps as scatter plot, there is no linear trend between the two variables, indicating that there is no correlation between them. Conclusion: after repeated vocal cord injury, the secretion of SP and VIP in vocal cord tissue increased. The biological effect of SP on vascular endothelial cells was that SP could directly act on the SP specific receptor on vascular endothelial cells to induce endothelium-dependent vasodilatory effect. By stimulating mast cells to release histamine, vasodilation can be induced indirectly by vasodilation, plasma exosmosis, and then local hyperemia and edema of vocal cord. VIP also has a strong vasodilation effect, and may increase the expression of vascular endothelial growth factor. In turn, it causes tissue edema. At the same time, SP and VIP can promote vasodilation, increase local blood supply of polyps, promote the release of inflammatory mediators from polyps, induce chronic inflammation, cause inflammatory cell infiltration, and damage vascular endothelial basement membrane. The increased permeability of peripheral blood vessels and the exudation of plasma proteins make some intravascular substances that are not easy to pass through the basement membrane enter the blood vessels, resulting in edema, dilatation, and high hydrostatic pressure of the lamina propria of the vocal cords. Therefore, the original pressure balance acting on the epigastric basement membrane was destroyed and the formation of vocal cord polyps was accelerated. This is also the theoretical basis for SP and VIP to participate in inflammatory reaction. The characteristics of neurogenic inflammation, I. e., SP and VIP, may increase in glands. Cystic dilatation plays an important role in promoting fibroblast proliferation and enhancing proliferation of fibroblasts induced by IL-1, resulting in vitreous degeneration, disorder of connective tissue arrangement in lamina propria, disappearance of lamellar structure and formation of polyps.
【学位授予单位】：昆明医学院
【学位级别】：硕士
【学位授予年份】：2010
【分类号】：R767.4

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