Abstract：
Cardiac microvascular endothelial cells (CMECs) are important cells surrounding the cardiomyocytes in the heart that maintain microenvironment homeostasis. Salvianic acid A sodium (SAAS) has been reported to prevent myocardial infarction (MI) injury. However, the role of SAAS on CMEC proliferation remains unclear. CEMCs exposed to oxygen glucose deprivation (OGD) were used to explore the angiogenic abilities of SAAS. In vivo, C57BL/6 mice were divided into three groups: sham, MI and SAAS + MI groups. Compared to OGD group, SAAS led to a reduction in the apoptotic rate and an increase of the proliferation in vitro. Additionally, SAAS increased the protein levels of Bcl2, HIF-1α and vascular endothelial growth factor (VEGF) with the reduction of Bax. In terms of the specific mechanisms, SAAS might inhibit HIF-1α ubiquitination and enhance the HIF-1α/VEGF signalling pathway to increase CMEC proliferation. Furthermore, SAAS increased the density of vessels, inhibited myocardial fibrosis and improved cardiac dysfunction in vivo. The present study has revealed that SAAS could potentially be used as an active substance to facilitate CMEC proliferation post-MI.
摘要：
心脏微血管内皮细胞（CMECs）是心脏心肌细胞周围维持微环境稳态的重要细胞。已经报道了丹参酸钠(SAAS)预防心肌梗塞(MI)损伤。然而,SAAS对CMEC增殖的作用尚不清楚.使用暴露于氧葡萄糖剥夺（OGD）的CEMC来探索SAAS的血管生成能力。在体内,将C57BL/6小鼠分为三组：假手术，MI和SAAS+MI组。与OGD组相比，SAAS导致体外凋亡率降低和增殖增加。此外,SAAS随Bax的降低而升高Bcl2、HIF-1α和血管内皮生长因子(VEGF)的蛋白水平。从具体机制来看,SAAS可能抑制HIF-1α泛素化并增强HIF-1α/VEGF信号通路以增加CMEC增殖。此外，SAAS增加了血管的密度，抑制心肌纤维化，改善体内心功能不全。本研究表明，SAAS可能用作促进MI后CMEC增殖的活性物质。
