Correlation analysis of epoxyeicosatrienoic acids with vascular endothelial dysfunction in senile diabetes mellitus

2011 ◽  
Vol 31 (3) ◽  
pp. 271-275
Author(s):  
Ya-li HUANG ◽  
Yan WANG ◽  
Xian DENG ◽  
Ruo-yu SHEN ◽  
Ling WU ◽  
...  
Endothelium ◽  
2004 ◽  
Vol 11 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Ming-Hui Zou ◽  
Richard A. Cohen ◽  
Volker Ullrich

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tomonori Akasaka ◽  
Seiji Hokimoto ◽  
Noriaki Tabata ◽  
Kenji Sakamoto ◽  
Kenichi Tsujita ◽  
...  

Background: Fluctuations in glucose levels give rise to inflammation and endothelial dysfunction by increasing oxidative stress. Mean amplitude of glycemic excursions (MAGE) is commonly used as a degree of fluctuations in glucose levels, and plays a significant role in vascular endothelial dysfunction in patient with diabetes mellitus (DM). Vascular endothelial dysfunction is associated with cardiovascular event risk. Thus, we examined the impact of MAGE on vascular endothelial dysfunction and clinical outcomes in non DM patients with CAD. Methods: We analyzed 22 non DM patients with CAD following percutaneous coronary intervention (PCI) during 12 months follow up, and assessed the relationship among MAGE, the level of high-sensitivity CRP (hs-CRP), and reactive hyperemia index (RHI) measured from RH-PAT (reactive hyperemia peripheral arterial tonometry). Cardiovascular events were cardiovascular death, myocardial infarction, stroke, unstable angina,and revascularization. Results: In clinical characteristics of total patients, age, HbA1c, average of blood glucose for 24 hour, and MAGE were 73ys, 5.93%, 121.5mg/dl, and 55.5mg/dl. MAGE correlated with hs-CRP (r=0.610; P=0.004) and RHI (r=–0.485; P=0.047), but not correlated with HbA1c, LDL cholesterol, HDL cholesterol, triglyceride, and systolic blood pressures. In short, high glycemic excursions (high MAGE) is associated with high inflammation (high hs-CRP) and vascular endothelial dysfunction (low RHI). When patients were classified into MAGE<60mg/dl (normal glycemic excursions) and MAGE>60mg/dl (high glycemic excursions), group of MAGE>60mg/dl were significant higher in hs-CRP (0.251±0.301 vs 0.072±0.067mg/dl, P=0.048) and lower in RHI (0.392±0.193 vs 0.834±0.316, P=0.008) than group of MAGE<60mg/dl. Multivariate analysis for vascular endothelial dysfunction identified MAGE as a predictive factor (OR13.3, 95%RI 1.069-166.4, P=0.044). Moreover, MAGE was an independent predictive factor for cardiovascular events (OR11.0, 95%RI 1.42-85.20, P=0.022) Conclusions: Fluctuations in glucose levels are associated with inflammation, endothelial dysfunction, and cardiovascular events risk in non DM patients with CAD.


2012 ◽  
Vol 10 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Dimitris Tousoulis ◽  
Anna-Maria Kampoli ◽  
Christodoulos Stefanadis

2020 ◽  
Vol 2 (2) ◽  
pp. 46-55
Author(s):  
Li X ◽  
Wu W ◽  
Wang Y ◽  
Zhang X ◽  
Feng X ◽  
...  

Objective: Liraglutide (LIRA), a Glucagon-like peptide-1 (GLP-1) receptor agonist, showed potential vascular protective effects with the mechanism remained incompletely understood. Therefore, this study aimed to investigate whether LIRA exerts its effect on vascular endothelial function in rats with type 2 diabetes mellitus (T2DM) via caveolin-1/ endothelial oxide synthase (eNOS) expression. Methods: T2DM rats were used as study subjects and randomly divided into four groups: 1) Veh group, 2) Veh+LIRA group, 3) T2DM group, and 4) T2DM+LIRA group. All rats received either saline or LIRA 0.2 mg/kg (by i.p. injection) per day for 4 weeks. After the model was successfully established, vascular endothelial function was determined the effect of vasodilator to mesenteric artery rings. Immunofluorescence and western blot were performed to understand the molecular mechanism. Cultured HUVECs with small interfering RNA (siRNA) under high glucose (HG), NO concentration, and western blot were performed to understand the molecular mechanism between LIRA and vascular endothelial function. Results: Based on our results, the LIRA reduced hyperglycemia and ameliorated vascular endothelial dysfunction in type 2 diabetic mice. LIRA activated eNOS phosphorylation, suppressing oxidative stress and enhancing endothelium-dependent vasorelaxation of mesenteric arteries. Besides, from its anti-oxidative capacity, LIRA activated eNOS to dilate the mesenteric arteries via the downregulation of Cav-1. Conclusion: LIRA ameliorates vascular endothelial dysfunction in rats with type 2 diabetes mellitus via anti-oxidative and activated eNOS by downregulated Cav-1.


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