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4-Hexylresorcinol-in duced angiogenesis potential in human endothelial cells

机译:4-己基间苯二酚在人内皮细胞中诱导血管生成潜力

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Background: 4-Hexylresorcinol (4HR) is able to increase angiogenesis. However, its molecular mechanism in the human endothelial cells has not been clarified.Methods: As endothelial cells are important in angiogenesis, we treated the human umbilical vein endothelial cells (HUVECs) with 4HR and investigated protein expressional changes by immunoprecipitation high-performance liquid chromatography (IP-HPLC) using 96 antisera.Results: Here, we found that 4HR upregulated transforming growth factor-beta (TGF-beta)/SMAD/vascular endothelial growth factor (VEGF) signaling, RAF-B/ERK and p38 signaling, and M2 macrophage polarization pathways. 4HR also increased expression of caspases and subsequent cellular apoptosis. Mechanistically, 4HR increased TGF-beta 1 production and subsequent activation of SMADs/VEGFs, RAF-B/ERK and p38 signaling, and M2 macrophage polarization.Conclusion: Collectively, 4HR activates TGF-beta/SMAD/VEGF signaling in endothelial cells and induced vascular regeneration and remodeling for wound healing.
机译:背景:4-己基间苯二酚(4HR)能够增加血管生成。然而,它在人内皮细胞中的分子机制尚未阐明。方法:由于内皮细胞在血管生成中很重要,我们用4HR处理人脐静脉内皮细胞(HUVECs),并使用96抗血清通过免疫沉淀高效液相色谱(IP-HPLC)研究蛋白质表达变化。结果:在这里,我们发现 4HR 上调转化生长因子-β (TGF-β)/SMAD/血管内皮生长因子 (VEGF) 信号传导、RAF-B/ERK 和 p38 信号传导以及 M2 巨噬细胞极化通路。 4HR 还增加了半胱天冬酶的表达和随后的细胞凋亡。从机制上讲,4HR 增加了 TGF-β 1 的产生和随后的 SMADs/VEGF、RAF-B/ERK 和 p38 信号传导以及 M2 巨噬细胞极化的激活。结论:4HR共同激活内皮细胞中的TGF-β/SMAD/VEGF信号传导,诱导血管再生和重塑,促进伤口愈合。

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