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作 者:陈飞[1] 乔祺[1] 王张生[1] 许澎[1] 陆刚[2]
机构地区:[1]复旦大学附属上海市第五人民医院心血管内科,上海200240 [2]复旦大学附属上海市第五人民医院急诊科,上海200240
出 处:《中国临床医学》2017年第2期166-170,共5页Chinese Journal of Clinical Medicine
摘 要:目的:观察丹参酮ⅡA磺酸钠(TanⅡA)对缺血性斑马鱼模型的促血管新生作用及其潜在机制。方法:用内皮细胞生长因子受体酪氨酸激酶抑制剂(VRKI)诱导血管损伤斑马鱼模型,分别予以50、100、200μmol/L的TanⅡA处理。观察TanⅡA在上述浓度下对缺血性斑马鱼肠下静脉血管(SIVs)和节间血管(ISVs)的影响,并利用real-time PCR技术检测flt-1、flk-1A(kdrl)、flk-1B(kdr)3个调节血管内皮生长因子(vascular endothelial growth factor,VEGF)信号通路相关基因的表达变化。结果:在VRKI诱导的血管损伤斑马鱼模型中,TanⅡA呈浓度依赖性地逐渐恢复ISVs和SIVs血管;通过VEGF通路上的相关基因[flt-1、flk-1A(kdrl)、flk-1B(kdr)]进行调控。结论:在缺血性斑马鱼模型中,TanⅡA可通过VEGF信号通路发挥其促血管新生和保护血管作用。Objective:To investigate the angiogenic effect and potential mechanism of sodium tanshinone Ⅱ A sulfonate(Tan Ⅱ A)in ischemic zebrafish model.Methods: Vascular endothelial growth factor receptor kinase inhibitor(VRKI)was used to induce vascular injury in zebrafish model.Then the ischemic zebrafish model was treated with 50,100,200μmol/L Tan Ⅱ A,respectively.The effects of Tan Ⅱ A on ischemic zebrafish subintestinal veins(SIVs)and intersegmental vessels(ISVs)were observed.Meanwhile,the expression changes of three vascular endothelial growth factor(VEGF)signaling pathway-related genes(flt-1,flk-1A,flk-1B)were detected by real-time PCR.Results:In VRKI-induced vascular injury zebrafish model,TanⅡA gradually restored ISVs and SIVs in a concentration-dependent manner,reversed the down-regulated expressions of three key VEGF signaling pathway-related genes(flt-1,flk-1A,flk-1B),and promoted angiogenesis.Conclusions:In the ischemic zebrafish model,Tan ⅡA plays a role in angiogenesis and vascular protection by regulating VEGF signaling pathway.
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