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背景与目的:肿瘤微生态系统的观点认为,由于肿瘤微生态系统内多因素相互作用产生的病理组织重构导致了肿瘤的病理学特征及生物学行为,血管内皮细胞生长因子(VEGF)对重构过程起着重要作用。本研究通过在体探索VEGF对神经胶质瘤组织重构的影响。方法:通过光镜和电镜观察转染有正义VEGFcDNA片段(C6/VEGF+),反义VEGFcDNA片段(C6/VEGF-)VEGF164,及转染有空载体的C6(C6/vec)的裸鼠移植瘤组织的形态结构,并检测不同肿瘤组织中VEGF的含量。结果:在转染C6/VEGF-的C6胶质瘤组织(C6/VEGF-G)中,VEGF含量及瘤周水肿明显低于转染C6/VEGF+和C6/vec的C6胶质瘤组织(C6/VEGF+G,C6/vecG)及的C6胶质瘤组织(C6G)(P<0.01,P<0.05),肿瘤组织的含水量与VEGF表达有相关性(r=0.791,P=0.000)。在C6/VEGF-G组中,肿瘤细胞表现出与血管壁结合不紧密,基板不连续、单层,外周见胶原纤维。但在C6G,C6/VEGF+和C6/vecG组中,肿瘤细胞通过自身延展紧密地黏附于血管壁;多数基质疏松,基板较完整连续,呈多层排列,外层见少量胶原纤维。血管内皮细胞胞浆内VVO样结构可见,VVO结构越多水肿越明显,VEGF表达水平与VVO数量呈明显相关(r=0.844,P=0.00);但VEGF表达与微血管内皮细胞孔窗无相关性,微血管内皮细胞孔窗及内皮细胞裂隙与瘤周水肿也无明显相关(r=0.01,P=0.970)。结论:VEGF通过内皮细胞内的VVO样结构增多加重肿瘤组织水肿。胶质瘤组织中瘤细胞对血管壁黏附性以及血管基板完整连续与否与VEGF表达有关。本研究揭示了胶质瘤组织重构的可能机制,以及阻断VEGF将有助于胶质瘤的治疗策略。
BACKGROUND & OBJECTIVE: From the perspective of the tumor micro-ecosystem, pathological tissue remodeling due to multi-factor interactions within the tumor micro-ecosystem leads to pathological features and biological behavior of the tumor. The effect of vascular endothelial growth factor (VEGF) Structural processes play an important role. This study explores the effect of VEGF on glioma tissue remodeling in vivo. METHODS: VEGF164 and C6 (C6 / vec) transfectants were transfected with the positive VEGFcDNA (C6 / VEGF +), antisense VEGFcDNA (C6 / VEGF-) Tissue morphology and structure, and detect different tumor tissue VEGF content. Results: The levels of VEGF and peritumoral edema in C6 / VEGF-G transfected C6 / VEGF-C6 cells were significantly lower than those in C6 / VEGF + and C6 / vec C6 C6 glioma tissues (P <0.01, P <0.05). There was a significant correlation between the water content and the expression of VEGF (r = 0.791, P = 0.000) in C6 glioma tissue (C6 / vegG / C6 / In the C6 / VEGF-G group, the tumor cells showed less binding to the vessel wall, discontinuous substrate, and monolayer and collagen fibers on the periphery. However, in the C6G, C6 / VEGF + and C6 / vecG groups, the tumor cells adhere closely to the vascular wall by self-extension; most of the matrix is loose and the substrate is more intact and continuous with multiple layers arranged with a few collagen fibers in the outer layer. VVO-like structure of vascular endothelial cells can be seen, VVO more edema structure more obvious, VEGF expression was significantly correlated with the number of VVO (r = 0.844, P = 0.00); but VEGF expression and microvascular endothelial cell pore window was not related , Microvascular endothelial cell pore window and endothelial cell fissure and peritumoral edema also had no significant correlation (r = 0.01, P = 0.970). Conclusion: VEGF increases the tumor tissue edema by increasing the VVO-like structure in endothelial cells. Glioma tissue tumor cells on the vascular wall adhesion and vascular integrity of the continuous or not and VEGF expression. This study reveals the possible mechanism of glioma tissue remodeling and blocking VEGF will contribute to the treatment strategy of glioma.