期刊
LIFE SCIENCES
卷 144, 期 -, 页码 86-93出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2015.06.010
关键词
Salvianolic acid A; Hypertension; Microvascular remodeling; Spontaneously hypertensive rats; Vascular endothelial function
资金
- National Natural Science Foundation of China [81173587]
- National Science and Technology Major Project for Key New Drug Creation and Manufacturing Program [2013ZX09103002-024]
- Shanghai Science and Technology Development Foundation [14401900900]
- Croucher Foundation [CAS14201]
Aims: Despite the numerous pharmacological agents available for hypertension therapy, hypertension-related microvascular remodeling is not resolved, eventually leading to end-organ damage. The aim of the present study was to investigate the protection of salvianolic acid A (SalA) against microvascular remodeling in vitro and in vivo. Main methods: Spontaneously hypertensive rats (SHRs) were administered 2.5, 5 or 10 mg/kg SalA via intraperitoneal injection once a day for 4 weeks. The tail-cuff method was applied to monitor blood pressure; the microvascular structure of the retina was detected by hematoxylin-eosin and immunohistochemical staining; the function of mesenteric arteries was measured by DMT wire myography; endothelial cell proliferation was estimated using the Cell Counting Kit-8; endothelial cell migration was evaluated by wound healing and transwell assay; and endothelial cell integrity was detected by transendothelial electrical resistance and permeability assays. Key findings: Although no antihypertensive effects of SalA were observed, SalA attenuated the microvascular inward remodeling of the retina and improved microvascular function in the mesenteries in vivo. Further cell experiments confirmed the beneficial effects of SalA on the integrity of the endothelial monolayer in vitro. Significance: Salvianolic acid A inhibited endothelial dysfunction and vascular remodeling in spontaneously hypertensive rats. Therefore, salvianolic acid A could be a potential drug therapy to prevent further targeted organ damage induced by vascular remodeling. (C) 2015 Published by Elsevier Inc.
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