Salvianolic acid A protects against vascular endothelial dysfunction in high-fat diet fed and streptozotocin-induced diabetic rats

被引:40
作者
Yang, Xiu-Ying [1 ,2 ]
Qiang, Gui-Fen [3 ]
Zhang, Li [1 ,2 ]
Zhu, Xiao-Ming [1 ,2 ]
Wang, Shou-Bao [1 ,2 ]
Sun, Lan [1 ,2 ]
Yang, Hai-Guang [1 ,2 ]
Du, Guan-Hua [1 ,2 ]
机构
[1] Chinese Acad Med Sci, Inst Mat Med, Beijing 100050, Peoples R China
[2] Peking Union Med Coll, Beijing 100050, Peoples R China
[3] Aerosp Ctr Hosp, Beijing 100049, Peoples R China
关键词
salvianolic acid A; diabetes; vascular endothelial dysfunction; oxidative stress; advanced glycation end products; NITRIC-OXIDE; EXPRESSION; CELLS; HYPERGLYCEMIA; REACTIVITY; STRESS; MODEL;
D O I
10.1080/10286020.2011.598457
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Salvianolic acid A (SalA) is one of the main active ingredients of Salvia miltiorrhizae. The objective of this study was to evaluate the effect of SalA on the diabetic vascular endothelial dysfunction (VED). The rats were given a high-fat and high-sucrose diet for 1 month followed by intraperitoneal injection of streptozotocin (30 mg/kg). The diabetic rats were treated with SalA (1 mg/kg, 90% purity) orally for 10 weeks after modeling, and were given a high-fat diet. Contractile and relaxant responses of aorta rings as well as the serum indications were measured. Our results indicated that SalA treatment decreased the level of serum Von Willebrand factor and ameliorated acetylcholine-induced relaxation and KCl-induced contraction in aorta rings of the diabetic rats. SalA treatment also reduced the serum malondialdehyde, the content of aortic advanced glycation end products (AGEs), and the nitric oxide synthase (NOS) activity as well as the expression of endothelial NOS protein in the rat aorta. Exposure of EA.hy926 cells to AGEs decreased the cell viability and changed the cell morphology, whereas SalA had protective effect on AGEs-induced cellular vitality. Our data suggested that SalA could protect against vascular VED in diabetes, which might attribute to its suppressive effect on oxidative stress and AGEs-induced endothelial dysfunction.
引用
收藏
页码:884 / 894
页数:11
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