Zhongwen Qi1, Meng Li2, Ke Zhu3, Junping Zhang4. 1. First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300183, China. Electronic address: 13820596855@163.com. 2. First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300183, China. 3. Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China. 4. First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300183, China. Electronic address: tjzhtcm@163.com.
Abstract
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.
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.
Authors: Siarhei A Dabravolski; Alexander M Markin; Elena R Andreeva; Ilya I Eremin; Alexander N Orekhov; Alexandra A Melnichenko Journal: Int J Mol Sci Date: 2022-10-01 Impact factor: 6.208