Vascular endothelial growth factor (VEGF) inhibition forms the basis for anti-angiogenic therapies. With the methods based on the monoclonal antibody-mediated typical VEGF blockade, pathological angiogenesis in the tumor microenvironment is inhibited and the limitation of tumor growth is provided; however, the existing tumor tissue cannot be intervened. In this study, the anti-angiogenic effects of Semaphorin (SEMA) 3F, which has frequently been reported to have tumor suppressive properties, on a chick chorioallantoic membrane model as well as in vitro cell-cell interactions were investigated and comparatively assessed using anti-VEGF antibody. Vascular endothelial cells and chick embryos were stimulated with 10-16 ng/mL VEGF165 prior to SEMA 3F administration in order to generate pathological vascularization conditions. Both in vitro and in ovo results revealed that SEMA 3F suppressed VEGF165-induced abnormal vascularization more effectively than anti-VEGF. Moreover, the required dose of SEMA 3F was significantly lower than that of anti-VEGF (103 times less under in ovo conditions). In light of these results, SEMA 3F is recommended as an important therapeutic agent for the prevention of pathological angiogenesis. SEMA 3F may offer an effective and efficient anti-angiogenic intervention that can be administered at a lower dose alternative to typical VEGF blocking agents.

中文翻译：

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Semaphorin 3F作为抗VEGF单克隆抗体的替代候选物对血管生成的抑制作用。

血管内皮生长因子（VEGF）抑制形成抗血管生成疗法的基础。采用基于单克隆抗体介导的典型VEGF阻断的方法，可抑制肿瘤微环境中的病理性血管生成，并提供了肿瘤生长的局限性。但是，现有的肿瘤组织无法介入。在这项研究中，Semaphorin（SEMA）3F对鸡绒囊尿囊膜模型的抗血管生成作用（经常被报道具有抑制肿瘤的作用）以及体外细胞与细胞之间的相互作用进行了研究，并使用抗VEGF抗体。在施用SEMA 3F之前，用10-16ng / mL VEGF165刺激血管内皮细胞和鸡胚，以产生病理性血管化条件。体外和卵内结果均显示，SEMA 3F比抗VEGF更有效地抑制VEGF165诱导的异常血管形成。此外，SEMA 3F的所需剂量显着低于抗VEGF的剂量（在卵内条件下的剂量低103倍）。根据这些结果，建议将SEMA 3F用作预防病理性血管生成的重要治疗剂。SEMA 3F可以提供有效且有效的抗血管生成干预措施，可以以较低剂量替代典型的VEGF阻断剂进行治疗。建议将SEMA 3F作为预防病理性血管生成的重要治疗剂。SEMA 3F可以提供有效且有效的抗血管生成干预措施，可以以较低剂量替代典型的VEGF阻断剂进行治疗。建议将SEMA 3F作为预防病理性血管生成的重要治疗剂。SEMA 3F可以提供有效且有效的抗血管生成干预措施，可以以较低剂量替代典型的VEGF阻断剂进行治疗。