2-Bromoethylamine protects vascular endothelium by inhibiting SSAO activity in diabetic rats.
- Author:
Zhen-Hua WANG
1
,
2
;
Chao-Sheng LI
;
Da-Hao YANG
;
Zheng-Rong XU
;
Jun-Hong CAI
;
Jun CHEN
Author Information
1. Institute of Graduate, Guangdong Medical College, Zhanjiang 524000, China
2. Cardiovascular Department, Shenzhen Bao'an People's Hospital, Shenzhen 518100, China. 896860112@qq.com.
- Publication Type:Journal Article
- MeSH:
Amine Oxidase (Copper-Containing);
metabolism;
Animals;
Aorta, Abdominal;
enzymology;
Diabetes Mellitus, Experimental;
enzymology;
Endothelin-1;
blood;
Endothelium, Vascular;
drug effects;
Ethylamines;
pharmacology;
Protective Agents;
pharmacology;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2014;66(4):476-482
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the change of aortic semicarbazide-sensitive amine oxidase (SSAO) activity in diabetic rats and examine the effect of 2-bromoethylamine (2-BEA) on SSAO activity and vascular endothelium in diabetic rats. SSAO was prepared from rat aorta. For assessment of the inhibitory effect, the enzymes were preincubated in the presence of different concentrations of 2-BEA before the addition of benzylamine in vitro. Type 1 diabetic rat model was induced by a single intraperitoneal injection of streptozotocin (STZ). Sprague Dawley (SD) rats were randomly divided into normal control group (NC), diabetic model group (DM), 2-BEA 5 mg/kg group, 2-BEA 20 mg/kg group (n = 10 in each group). 2-BEA was administered daily via intraperitoneal injection for 8 weeks. At the end of 8 weeks, blood sample was collected from the abdominal aorta. Plasma nitric oxide (NO) was determined by nitrate reductase method. Plasma endothelin-1 (ET-1) was determined by radioimmunoassay. Aorta SSAO was determined by high performance liquid chromatography. The aorta was prepared to observe morphological changes and ultramicroscopic structures. The results were as follows: Compared with NC group, aortic SSAO activity and the plasma ET-1 were significantly increased (P < 0.01), and plasma NO was significantly decreased (P < 0.01) in DM group. 2-BEA decreased plasma ET-1 and elevated plasma NO by inhibiting aortic SSAO activity in diabetic rats (P < 0.01), and 2-BEA 20 mg/kg group was more significant than 2-BEA 5 mg/kg group (P < 0.05). Endothelial injury of 2-BEA group rats was less serious than DM group. These results suggest that 2-BEA protect aortic endothelium by inhibiting aortic SSAO activity.
