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Different effects of catechin on angiogenesis and inflammation depending on VEGF levels

机译:儿茶素对血管生成和炎症的影响取决于VEGF水平

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Although physiological and pathological angiogenesis develop through similar processes, during pathological angiogenesis, proangiogenic factors are exacerbated. Polyphenols have been considered therapeutic tools for conditions exhibiting enhanced angiogenesis. However, the possibility that these compounds may also prevent vascularization in physiological situations is a major drawback for their use. The purpose of the current study was to investigate the effects of 0.1-100 mu M catechin on endothelial cells (EC) and vascular smooth muscle cells (VSMC) regarding angiogenic and inflammatory processes. Catechin modulation of angiogenesis and inflammation was also evaluated in vivo using different models of angiogenesis: one physiological (skin wound-healing assay) and another one resembling pathological angiogenesis, exhibiting higher vascular endothelial growth factor (VEGF)-A stimulation (Matrigel plug assay). The in vitro results showed that 100 mu M catechin increased viability (to 165.58% and to 165.34%) and decreased apoptosis (53.45% and 92.65%) and proliferation (33.19% and 23.36%) of EC and VSMC, respectively. Catechin affected migration and invasion, tending to increase both in EC and decreasing them in VSMC; however, it did not change sprouting angiogenesis. Nevertheless, catechin diminished in vitro inflammatory modulators such as tumor necrosis factor alpha (58.66% for human umbilical vein endothelial cells and 85.46% for human aortic smooth muscle cells) and nuclear factor kappa-B (38.43% for VSMC). The in vivo results demonstrated that catechin did not change angiogenesis and inflammation in skin wound-healing model and substantially decreased these processes in Matrigel plug assay. Altogether, the current study showed that catechin has different effects in angiogenesis and inflammation depending on VEGF-A levels. The absence of adverse effects in mature vasculature favors catechin potential use against pathological situations where angiogenesis is stimulated. (c) 2013 Elsevier Inc. All rights reserved.
机译:尽管生理和病理性血管生成通过相似的过程发展,但是在病理性血管生成期间,促血管生成因子加剧。多酚已被认为是用于表现出增强的血管生成的疾病的治疗工具。但是,这些化合物在生理情况下也可能阻止血管形成的可能性是其使用的主要缺点。本研究的目的是研究0.1-100μM儿茶素对血管生成和炎症过程对内皮细胞(EC)和血管平滑肌细胞(VSMC)的影响。还使用不同的血管生成模型在体内评估了儿茶素对血管生成和炎症的调节作用:一种生理学(皮肤伤口愈合分析)和另一种类似于病理性血管生成的模型,表现出更高的血管内皮生长因子(VEGF)-A刺激作用(基质胶塞分析) 。体外结果表明,100μM儿茶素分别提高EC和VSMC的活力(分别达到165.58%和165.34%)并降低凋亡(分别为53.45%和92.65%)和增殖(分别为33.19%和23.36%)。儿茶素影响迁移和侵袭,在EC中趋于增加,而在VSMC中趋于降低。然而,它并没有改变发芽的血管生成。然而,儿茶素减少了体外炎症调节剂,例如肿瘤坏死因子α(人脐静脉内皮细胞为58.66%,人主动脉平滑肌细胞为85.46%)和核因子κB(VSMC为38.43%)。体内结果表明,儿茶素不会改变皮肤伤口愈合模型中的血管生成和炎症,并在Matrigel塞栓试验中显着减少了这些过程。总而言之,当前的研究表明,儿茶素在血管生成和炎症中的作用取决于VEGF-A的水平。在成熟的脉管系统中不存在不良影响,有利于儿茶素潜在地用于刺激血管生成的病理情况。 (c)2013 Elsevier Inc.保留所有权利。

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