期刊
CARDIOVASCULAR DIABETOLOGY
卷 11, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1475-2840-11-94
关键词
Telmisartan; Adiponectin receptor; NADPH oxidase; Type 2 diabetic; Cardiac; Aorta
资金
- Shanxi Scholarship Council of China [2007-44, 2011-48]
- Department of Personnel of Shanxi Province of China
Background: Diabetic cardiovascular disease is associated with decreased adiponectin and increased oxidative stress. This study investigated the effect of telmisartan on the expression of adiponectin receptor 2 (adipoR2) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits in the heart and the expression of adiponectin receptor 1 (adipoR1) in aorta in type 2 diabetic rats. Methods: Type 2 diabetes was induced by high-fat and high-sugar diet and intraperitoneal injection of a low dose of streptozotocin (STZ). Heart function, adipoR2, p22phox, NOX4, glucose transporter 4(GLUT4), monocyte chemoattractant protein-1(MCP-1) and connective tissue growth factor (CTGF) in the heart, and adipoR1, MCP-1 and nuclear factor kappa B (NF-kappa B) in aorta were analyzed in controls and diabetic rats treated with or without telmisartan (5mg/kg/d) by gavage for 12 weeks. Results: Heart function, plasma and myocardial adiponectin levels, the expression of myocardial adipoR2 and GLUT4 were significantly decreased in diabetic rats (P<0.05). The expression of myocardial p22phox, NOX4, MCP-1, and CTGF was significantly increased in diabetic rats (P<0.05). The expression of adipoR1 was decreased and the expression of MCP-1 and NF-kB was increased in the abdominal aorta in diabetic rats (P<0.05). Telmisartan treatment significantly attenuated these changes in diabetic rats (P<0.05). Conclusions: Our results suggest that telmisartan upregulates the expression of myocardial adiponectin, its receptor 2 and GLUT4. Simultaneously, it downregulates the expression of myocardial p22phox, NOX4, MCP-1, and CTGF, contributing so to the improvement of heart function in diabetic rats. Telmisartan also induces a protective role on the vascular system by upregulating the expression of adipoR1 and downregulating the expression of MCP-1 and NF-kappa B in the abdominal aorta in diabetic rats.
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