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目的了解血管内皮细胞生长因子(VEGF)对胶质瘤病理形态的影响。方法利用光镜和电镜观察转染有反义VEGF cDNA片段的C_6胶质瘤细胞的裸鼠移植瘤的病理特征,ELISA法检测肿瘤组织中VEGF的含量。结果转染有反义VEGF cDNA片段的C_6胶质瘤组织中VEGF含量明显低于仅转染有空载体的C_6胶质瘤组织(P＜0．05)。前者瘤组织表面存在类包膜,瘤周血管反应轻。无明显瘤周水肿,瘤周侵袭少见,凋亡瘤细胞明显增多；血管内皮细胞胞浆内VVO样结构少见,基板不连续、单层,外周见胶原纤维；但个别肿瘤大者瘤组织中VEGF含量也高,且内皮细胞VVO样结构也随之增多。而后者瘤周血管反应明显,瘤体和瘤周水肿严重,瘤细胞可侵袭瘤周组织,瘤内组织明显出血坏死,且可见瘤细胞形成类微血管样结构,血管内皮细胞胞浆内VVO样结构较多,水肿越明显VVO样结构越多见,并与组织中VEGF含量相一致；基板较完整连续,多数基质疏松,呈多层排列,外层见少量胶原纤维。所观察的几种肿瘤中的微血管内皮细胞孔窗及内皮细胞裂隙与转染的目的基因无明显的关系,且内皮细胞的凋亡均不明显。结论胶质瘤细胞上VEGF表达的下调可促进胶质瘤细胞凋亡；VEGF通过内皮细胞内的VVO样结构增多引起血管渗透性增加致瘤体和瘤周水肿,而与内皮细胞上孔窗无明显的关系：胶质瘤组织中的血管基板完整连续与否与VEGF有关。
Objective To investigate the effect of vascular endothelial growth factor (VEGF) on the pathology of glioma. Methods The pathological characteristics of C_6 glioma cells transfected with antisense VEGF cDNA fragments were observed by light and electron microscopy. The content of VEGF in tumor tissues was detected by ELISA. Results The VEGF content in C_6 glioma transfected with antisense VEGF cDNA was significantly lower than that in C_6 glioma transfected with empty vector (P <0.05). The former tumor-like surface of the envelope, peritumoral vascular response to light. There were no significant peritumoral edema, rare peritumoral invasion and a marked increase of apoptotic tumor cells. VVO-like structures in vascular endothelial cells were rare, and the basal plate was not continuous, monolayer and peripheral collagen fibers were found. However, the expression of VEGF The content is also high, and endothelial VVO-like structure also increased. While the latter had obvious peritumoral vascular response. The tumor and peritumoral edema were serious. The tumor cells could invade the peritumoral tissue and the hematogenous tissues were obviously hemorrhagic and necrotic. The tumor-like microvascular-like structure and the intracellular VVO-like structure of vascular endothelial cells More, the more obvious edema VVO-like structure, the more common and consistent with the content of VEGF in the tissue; substrate more complete continuity, most of the matrix loose, were arranged in layers, the outer layer see a small amount of collagen fibers. There was no significant relationship between the cell window and the endothelial cell fissure of the microvascular endothelial cells observed in several tumors and the transfected gene, and the apoptosis of endothelial cells was not obvious. Conclusions The down-regulation of VEGF expression in glioma cells can promote the apoptosis of glioma cells. Increasing of VVO-like structure in endothelial cells leads to the increase of vascular permeability to tumor and peritumoral edema, but not to that of endothelial cells Obvious relationship: glioma tissue in the vascular continuity or not and VEGF-related.