Si-Miao-Yong-An on promoting the maturation of Vasa Vasorum and stabilizing atherosclerotic plaque in ApoE-/- mice : An experimental study
Si-Miao-Yong-An on promoting the maturation of Vasa Vasorum and stabilizing atherosclerotic plaque in ApoE-/- mice : An experimental study
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DOI：
10.1016/j.biopha.2019.108785
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发表时间：
2019-06-01
影响因子：
7.5
通讯作者：
Zhang, Junping
中科院分区：
文献类型：
--
作者：
Qi, Zhongwen;Li, Meng;Zhang, Junping
目的：为观察四妙永安（SMYA）对动脉粥样硬化（AS）易损斑块的干预作用，并以血管成熟为切入点探讨其作用机制，材料与方法：SPF级健康雄性ApoE（-/-）小鼠随机分为模型组、SMYA组和辛伐他汀组，以C57 BL/6小鼠为对照组。药物干预8周后，HE染色观察AS斑块。应用免疫荧光双染色（CD 34、Desmin）及VV密度法观察主动脉根部斑块周细胞。结果：参麦雅片能显著减少ApoE（-/-）小鼠主动脉斑块面积，降低斑块面积和斑块与管腔面积比，降低内膜中层厚度，其作用大于辛伐他汀;能显著增加斑块内VV密度。结论：SMYA能减少ApoE（-/-）小鼠AS斑块面积，促进VV周细胞的募集，稳定AS易损斑块。其机制可能与Dll 4/Notch 1/Hey 1/VEGF信号通路的调节有关。同时对VV具有双向调节。
Objective: To observe the intervention effect of Si-miao-Yong-An (SMYA) on atheroosclerosis (AS) vulnerable plaque, and to explore the mechanism by Vasa Vasorum (VV) maturation as a starting point.Materials and methods: SPF-class healthy male ApoE(-/-) mice were randomly divided into model group, SMYA group and simvastatin group, and C57BL/6 mice were used as a control group. After 8 weeks of drug intervention, the plaques of AS were observed by HE staining. The pericytes of aortic root plaques were observed by immunofiuorescence double staining (CD34, Desmin) and the density of VV. The expression of Dll4, Notch1, Hey1 and VEGF mRNA in aortic tissues was detected by real-time qPCR.Results: SMYA significantly reduced the area of aortic plaque in ApoE(-/-) mice, significantly reduced plaque area and the ratio of plaque to lumen area, and reduced the intima medium thickness, it's effect was greater than that of simvastatin; it significantly increased the density of VV in plaque. SMYA increased the expression of Dll4 and Notch1 and Hey1mRNA, and decreased the expression of VEGF mRNA, and its effect was greater than that of simvastatin.Conclusion: SMYA can reduce the AS plaque area in ApoE(-/-) mice, promote the recruitment of VV pericytes, and stabilize AS vulnerable plaques. The mechanism may be regulate of Dll4/Notch1/ Hey1/VEGF signaling pathway. At the same time, it has a dual-direction regulation on the VV.