Ameliorative effect of astaxanthin on endothelial dysfunction in streptozotocin-induced diabetes in male rats

被引:7
|
作者
Zhao, Zi-Wen
Cai, Wei
Lin, Yun-Ling
Lin, Qing-Fei
Jiang, Qiong
Lin, Zhang
Chen, Liang-Long [1 ]
机构
[1] Fujian Med Univ, Union Hosp, Dept Cardiol, Fuzhou 350001, Peoples R China
来源
ARZNEIMITTEL-FORSCHUNG-DRUG RESEARCH | 2011年 / 61卷 / 04期
关键词
Astaxanthin; Diabetes; Endothelial dysfunction; Endothelial nitric oxide synthase; Lectin-like oxidized low-density lipoprotein receptor-1; Oxidative stress; LOW-DENSITY-LIPOPROTEIN; NITRIC-OXIDE SYNTHASE; HIGH-FAT DIET; LECTIN-LIKE; OXIDATIVE STRESS; RECEPTOR-1; LOX-1; CARDIOVASCULAR-DISEASE; ICAM-1; EXPRESSION; MONOCYTE ADHESION; LDL RECEPTOR-1;
D O I
暂无
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The present study was designed to examine whether astaxanthin (ASX, 3,3-dihydroxybeta, beta-carotene-4,4-dione, CAS 472-61-7), a dietary antioxidant carotenoid that is naturally present in algae, crustaceans, and fish, has a protective effect on endothelial dysfunction of aortas in diabetic rats and the possible molecular mechanism involved. Male Wistar rats were randomly divided into four groups: control rats, diabetic rats, diabetic rats treated with ASX (10 mg/kg/d), and control rats treated with ASX. Type 1 diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ; 60 mg/ kg). STZ-induced diabetes in rats was complicated with excessive oxidative stress and endothelial dysfunction, increased serum oxidized low-density lipoprotein (ox-LDL) and aortic malondialdehyde (MDA) levels, inhibited endothelium-dependent vasorelaxation to acetylcholine (ACh) and unaffected endothelium-dependent vasorelaxation to sodium nitroprusside (SNP). Simultaneously, lectin-like oxLDL receptor-1 (LOX-1) expression was enhanced and endothelial nitric oxide (NO) synthase (eNOS) expression was reduced in the aortas of diabetic rats. ASX treatment could significantly decrease serum oxLDL and aortic MDA levels, attenuate blunted endothelium-dependent vasodilator responses to ACh, upregulate eNOS expression, and decrease LOX-1 expression. These results indicated that ASX could ameliorate diabetic endothelial dysfunction by inhibiting the ox-LDLLOX-1-eNOS pathway. Treatment with ASX might be clinically useful for diabetic complications associated with endothelial dysfunction.
引用
收藏
页码:239 / 246
页数:8
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