EGFR及VEGF在声带息肉中的表达

发布时间：2018-08-12 12:00

【摘要】：目的：检测表皮生长因子受体(epidermal growth factor receptor, EGFR)及血管内皮生长因子(vascular endothelial growth factor, VEGF)在正常声带组织和声带息肉中的表达,了解EGFR及VEGF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,为临床防治提供理论依据。方法：选取经病理诊断确诊,且排除其它声带病变的声带息肉患者标本37例为实验组。取正常声带组织标本11例为对照组。所有标本经HE染色后,进行Max VisionTM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,EGFR及VEGF的表达均较弱,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EGFR阳性单位均值(19.2109±9.1636)高于正常声带组(7.2125±4.2481),有统计学差异(p0.05)。声带息肉组VEGF阳性单位均值(33.5317±6.1559)高于正常声带组(18.9507±5.5183),也有统计学差异(p0.05)。用声带息肉中EGFR及VEGF的阳性单位均值做散点图,两变量之间不存在线性关系,说明二者没有相关性。结论：①声带息肉是多因素共同作用的结果,各种原因导致反复的声带损伤,引起局部充血、水肿、出血,黏膜上皮变性、坏死、脱落、增生,炎性细胞浸润,血管增生、扩张。②声带在长期的损伤过程中,由于EGFR及VEGF与其它相关炎性介质的共同作用导致慢性炎症,血管内皮基底膜受损、血管壁通透性增强,一些本来不易通过血管壁的血管内物质进入组织间隙,导致声带黏膜固有层,特别是Reinke's间隙水肿、炎性细胞浸润、纤维细胞增生、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。③声带息肉发展过程中,EGFR及VEGF同时促进息肉血管的形成,息肉血管增生,息肉获得丰富的血供从而不断生长。④VEGF在声带损伤中,介导细胞外基质的降解与重构,沉积于声带组织中,降低声带弹性,这也是声带息肉发生发展的因素之一。当体外某些刺激因素使EGFR过度表达时,则持续向细胞内传递分裂增殖信号,导致DNA合成增加,刺激各种细胞持续增长和增殖,形成息肉。
[Abstract]:Objective: To investigate the expression of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) in normal vocal cord tissues and vocal cord polyps, and to investigate the effect of EGFR and VEGF on the pathogenesis of vocal cord polyps. Methods: 37 cases of vocal cord polyps diagnosed by pathology and excluding other vocal cord lesions were selected as the experimental group, and 11 cases of normal vocal cord tissues as the control group. The expression of EGFR and VEGF was weaker in normal vocal cords, but stronger in epithelial cells, inflammatory cells, vascular endothelial cells, glandular cells and fibroblasts in polyps of vocal cords. The mean value of EGF positive unit was higher than that of normal vocal cord group (33.5317+6.1559) and the difference was statistically significant (p0.05). There was no linear relationship between the two variables. Conclusion: 1. Vocal cord polyps were the result of multi-factor interaction. The cause is repeated vocal cord injury, causing local congestion, edema, hemorrhage, mucosal epithelial degeneration, necrosis, exfoliation, hyperplasia, inflammatory cell infiltration, vascular proliferation, dilatation. 2 Vocal cords in the long-term injury process, due to EGFR and VEGF and other related inflammatory mediators in the joint role of chronic inflammation, vascular endothelial basement membrane damage, vascular wall. Increased permeability, some of the vascular substances originally difficult to enter the tissue space through the vascular wall, resulting in vocal cord mucosa lamina propria, especially Reinke's space edema, inflammatory cell infiltration, fibrocyte proliferation, hyaline degeneration, laminar structure disappeared, polyp formation. GFR and VEGF promote the formation of polyp blood vessels, polyp blood vessels proliferation, polyps get rich blood supply and thus continue to grow. When GFR is overexpressed, it continuously transmits divisive and proliferative signals to cells, resulting in increased DNA synthesis, stimulating the sustained growth and proliferation of various cells, forming polyps.
【学位授予单位】：昆明医科大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R767.4

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