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丹酚酸A对高脂饮食喂养和链脲佐菌素诱导的糖尿病大鼠的血管内皮功能障碍具有保护作用。

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

作者信息

Yang Xiu-Ying, Qiang Gui-Fen, Zhang Li, Zhu Xiao-Ming, Wang Shou-Bao, Sun Lan, Yang Hai-Guang, Du Guan-Hua

机构信息

Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

出版信息

J Asian Nat Prod Res. 2011 Oct;13(10):884-94. doi: 10.1080/10286020.2011.598457.

DOI:10.1080/10286020.2011.598457
PMID:21972802
Abstract

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.

摘要

丹酚酸A(SalA)是丹参的主要活性成分之一。本研究的目的是评估SalA对糖尿病血管内皮功能障碍(VED)的影响。大鼠给予高脂高糖饮食1个月,随后腹腔注射链脲佐菌素(30 mg/kg)。建模后,糖尿病大鼠口服SalA(1 mg/kg,纯度90%)治疗10周,并给予高脂饮食。测量主动脉环的收缩和舒张反应以及血清指标。我们的结果表明,SalA治疗降低了糖尿病大鼠血清血管性血友病因子水平,改善了乙酰胆碱诱导的主动脉环舒张和氯化钾诱导的收缩。SalA治疗还降低了大鼠血清丙二醛、主动脉晚期糖基化终产物(AGEs)含量、一氧化氮合酶(NOS)活性以及主动脉内皮型NOS蛋白的表达。将EA.hy926细胞暴露于AGEs会降低细胞活力并改变细胞形态,而SalA对AGEs诱导的细胞活力具有保护作用。我们的数据表明,SalA可以预防糖尿病中的血管VED,这可能归因于其对氧化应激和AGEs诱导的内皮功能障碍的抑制作用。

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