Curculigoside A induces angiogenesis through VCAM-1/Egr-3/CREB/VEGF signaling pathway

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• 作者：Z. Kang^a ; H. Zhu^b ; H. Luan^a ; F. Han^a ; ; W. Jiang^a ; ^{jwl518@163.com" class="auth_mail}
• 关键词：CREB ; cAMP response element-binding protein ; DMEM ; Dulbecco&rsquo ; s Modified Eagle Medium ; EDTA ; ethylenediaminetetraacetic acid ; Egr-3 ; early growth response 3 ; ELISA ; enzyme-linked immunosorbent assay ; FBS ; fetal bovine serum ; HBMEC ; human brain microvascular endothelial cell line ; HEPES ; hydroxyethyl piperazineethanesulfonic acid ; LDH ; lactate dehydrogenase ; MTT ; 3-(4 ; 5-dimethylthiazol-2-yl)-2 ; 5-diphenyltetrazolium bromide ; p-CREB ; phosphor-CREB ; PCNA ; proliferating cell nuclear antigen ; VCAM
• 刊名：Neuroscience
• 出版年：16 May, 2014
• 年：2014
• 卷：267
• 期：Complete
• 页码：232-240
• 全文大小：949 K

文摘

Curculigoside A may be a powerful way of protecting the brain against a wide variety of injury. In the present study, we sought to elucidate whether Curculigoside A contributes to induce angiogenesis and its mechanisms. To this end, we examined the role of Curculigoside A on proliferation, invasion, and tube formation in the human brain microvascular endothelial cell line (HBMEC) in vitro. For studying mechanism, the cAMP response element-binding protein (CREB) inhibitor 2-naphthol-AS-E-phosphate (KG-501), early growth response 3 (Egr-3) siRNA, vascular endothelial growth factor (VEGF) antagonist sFlt-1 and VEGF receptor 2 (VEGFR2) blocker SU-1498 were used. Human brain microvascular endothelial cell line (HMBEC) proliferation was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Scratch adhesion test was used to assess the ability of invasion. A matrigel tube formation assay was performed to test capillary tube formation ability. Vascular cell adhesion molecule 1 (VCAM-1)/Egr-3/CREB/VEGF pathway activation in HMBEC was tested by Western blot analysis. Our data suggested that Curculigoside A induced angiogenesis in vitro by enhancing the proliferation, invasion and tube formation. VEGF expression was increased by Curculigoside A and counteracted by the soluble VEGF receptor 1 (sFlt-1, VEGF antagonist) and KG-501 in HMBEC. Tube formation was enhanced by Curculigoside A and counteracted by VEGF receptor blocker-SU1498, KG-501 and Egr-3 siRNA. It may be suggested that Curculigoside A induces angiogenesis in vitro via a programed VCAM-1/Egr-3/CREB/VEGF signaling axis.