AUTONOMIC AND ENDOTHELIAL DYSFUNCTION IN EXPERIMENTAL DIABETES

2000 ◽  
Vol 22 (6) ◽  
pp. 623-634 ◽  
Author(s):  
B. Martínez-Nieves ◽  
H. L. Collins ◽  
S. E. DiCarlo
2015 ◽  
Vol 93 (7) ◽  
pp. 555-561 ◽  
Author(s):  
Adrian Sturza ◽  
Oana M. Duicu ◽  
Adrian Vaduva ◽  
Maria D. Dănilă ◽  
Lavinia Noveanu ◽  
...  

Diabetes mellitus (DM) is widely recognized as the most severe metabolic disease associated with increased cardiovascular morbidity and mortality. The generation of reactive oxygen species (ROS) is a major event causally linked to the development of cardiovascular complications throughout the evolution of DM. Recently, monoamine oxidases (MAOs) at the outer mitochondrial membrane, with 2 isoforms, MAO-A and MAO-B, have emerged as novel sources of constant hydrogen peroxide (H2O2) production in the cardiovascular system via the oxidative deamination of biogenic amines and neurotransmitters. Whether MAOs are mediators of endothelial dysfunction in DM is unknown, and so we studied this in a streptozotocin-induced rat model of diabetes. MAO expression (mRNA and protein) was increased in both arterial samples and hearts isolated from the diabetic animals. Also, H2O2 production (ferrous oxidation – xylenol orange assay) in aortic samples was significantly increased, together with an impairment of endothelium-dependent relaxation (organ-bath studies). MAO inhibitors (clorgyline and selegiline) attenuated ROS production by 50% and partially normalized the endothelium-dependent relaxation in diseased vessels. In conclusion, MAOs, in particular the MAO-B isoform, are induced in aortas and hearts in the streptozotocin-induced diabetic rat model and contribute, via the generation of H2O2, to the endothelial dysfunction associated with experimental diabetes.


2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S30.3-S30 ◽  
Author(s):  
A Sturza ◽  
L Noveanu ◽  
O Duicu ◽  
DM Muntean

2019 ◽  
Vol 38 (8) ◽  
pp. 962-973 ◽  
Author(s):  
JS Hussein ◽  
W Rasheed ◽  
T Ramzy ◽  
M Nabeeh ◽  
M Harvy ◽  
...  

Objective: To investigate the ability of docosahexaenoic acid (DHA)-loaded silver nanoparticles (AgNPs) in facilitating the incorporation of DHA in the cell membrane, improve cell membrane structure, and attenuate endothelial dysfunction in experimental diabetes. Methods: DHA/AgNPs were prepared using a nanoprecipitation technique. Fifty male albino rats were used in this study; 10 of them were served as the control group and 40, as the experimental groups, were injected with streptozotocin. Then, the experimental groups were subdivided into diabetic, diabetic treated with DHA, diabetic treated with AgNPs, and diabetic treated with DHA/AgNPs groups. Results: DHA/AgNPs have small spherical size as proved from ultraviolet–visible spectroscopy, transmission electron microscope, dynamic light scattering, and scanning electron microscope techniques. Cell membrane cholesterol and triglycerides showed a significant elevation in the diabetic group compared to the control, but treatment with DHA and DHA/AgNPs caused a significant reduction in both. Treatment with AgNPs and DHA/AgNPs caused a significant improvement in asymmetric dimethylarginine and nitric oxide levels compared to the diabetic group. Cell membrane fatty acids showed that omega-6 polyunsaturated fatty acids (PUFAs) were significantly elevated, while omega-3 PUFA were significantly reduced in the diabetic group compared to the control. There is a significant improvement in the levels of fatty acids in all groups after treatment with DHA, silver, or DHA/AgNPs. Conclusion: DHA/AgNPs are potent agents for the improvement of diabetic complication and endothelial dysfunction in experimental diabetes.


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