Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, 100078, People's Republic of China.
The Third Affiliated Hospital, Beijing University of Chinese Medicine, Beijing, 100029, People's Republic of China.
Drug Des Devel Ther. 2023 Nov 7;17:3249-3267. doi: 10.2147/DDDT.S426345. eCollection 2023.
Combination of L and Bunge. (PS) has been widely used in the clinical treatment of ischemic heart disease. The purpose of this study was to explore the therapeutic effect and mechanism of PS on angiogenesis in rats after acute myocardial infarction (AMI).
A rat model of AMI was established by ligating the left anterior descending (LAD) artery. The grouping and administration scheme were as follows: sham group, model group, PS low-dose (PS-L) group, PS high-dose (PS-H) group, PX-478 group and angiotensin converting enzyme inhibitor (ACEI) group. After 28 days of treatment, echocardiography, myocardial infarct size, some angiogenesis markers and the miR-155-5p/HIF-1α/VEGF axis were measured.
PS improved cardiac structure and function, reduced infarct size, and alleviated myocardial fibrosis and inflammatory cell infiltration in AMI rats. Mechanistically, PS enhanced the expression of HGF and bFGF in serum, increased the levels of MVD and CD31 in myocardial tissues, and inhibited the activation of the miR-155-5p/HIF-1α/VEGF pathway, which ultimately promoted angiogenesis. In addition, the regulatory effect of PS on angiogenesis was partly abolished by PX-478.
PS increased the expression of MVD and CD31 in the myocardium and stimulated angiogenesis. The above effects of PS may be associated with the inhibition of the miR-155-5p/HIF-1α/VEGF axis.
L 和 Bunge 的组合（PS）已广泛用于缺血性心脏病的临床治疗。本研究旨在探讨 PS 对急性心肌梗死（AMI）大鼠血管生成的治疗作用及其机制。
结扎左前降支（LAD）建立大鼠 AMI 模型。分组和给药方案如下：假手术组、模型组、PS 低剂量（PS-L）组、PS 高剂量（PS-H）组、PX-478 组和血管紧张素转化酶抑制剂（ACEI）组。治疗 28 天后，行超声心动图检查，测量心肌梗死面积、部分血管生成标志物及 miR-155-5p/HIF-1α/VEGF 轴。
PS 改善了 AMI 大鼠的心脏结构和功能，减少了梗死面积，减轻了心肌纤维化和炎症细胞浸润。机制上，PS 增强了血清中 HGF 和 bFGF 的表达，增加了心肌组织中 MVD 和 CD31 的水平，并抑制了 miR-155-5p/HIF-1α/VEGF 通路的激活，最终促进了血管生成。此外，PS 对血管生成的调节作用部分被 PX-478 所阻断。
PS 增加了心肌中 MVD 和 CD31 的表达，刺激了血管生成。PS 的上述作用可能与抑制 miR-155-5p/HIF-1α/VEGF 轴有关。
