scholarly journals Healthberry 865® and Its Related, Specific, Single Anthocyanins Exert a Direct Vascular Action, Modulating Both Endothelial Function and Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1191
Author(s):  
Albino Carrizzo ◽  
Rosario Lizio ◽  
Paola Di Pietro ◽  
Michele Ciccarelli ◽  
Antonio Damato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Intracellular Signaling ◽  
Vascular Reactivity ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Epidemiological Studies ◽  
Direct Role ◽  
And Oxidative Stress

In recent years, epidemiological studies have identified a relationship between diet and cerebro–cardiovascular disease (CVD). In this regard, there is a promising dietary group for cardiovascular protection are polyphenols, especially anthocyanins. Vascular reactivity studies were performed using Healthberry 865® and constituent single anthocyanins to characterize vasomotor responses; immunofluorescence analysis with dichlorofluorescein diacetate and dihydroethidium were used to evaluate nitric oxide and oxidative stress; lucigenin assay was used to measure NADPH oxidase activity; and gel electrophoresis and immunoblotting were used to dissect the molecular mechanisms involved. We demonstrated that Healthberry 865® exerts an important vasorelaxant effect of resistance artery functions in mice. Its action is mediated by nitric oxide release through the intracellular signaling PI3K/Akt. Moreover, behind its capability of modulating vascular tone, it also exerts an important antioxidant effect though the modulation of the NADPH oxidase enzyme. Interestingly, its cardiovascular properties are mediated by the selective action of different anthocyanins. Finally, the exposure of human dysfunctional vessels to Healthberry 865® significantly reduces oxidative stress and improves NO bioavailability. Although further investigations are needed, our data demonstrate the direct role of Healthberry 865® on the modulation of vasculature, both on the vasorelaxation and on oxidative stress; thus, supporting the concept that a pure mixture of anthocyanins could be helpful in preventing the onset of vascular dysfunction associated with the development of CVD.

scholarly journals Arginine therapy of transgenic-knockout sickle mice improves microvascular function by reducing non-nitric oxide vasodilators, hemolysis, and oxidative stress

2008 ◽  
Vol 295 (1) ◽  
pp. H39-H47 ◽  
Author(s):  
Dhananjay K. Kaul ◽  
Xiaoqin Zhang ◽  
Trisha Dasgupta ◽  
Mary E. Fabry
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Vascular Reactivity ◽  
Microvascular Function ◽  
Cell Disease ◽  
No Bioavailability ◽  
Cox 2 ◽  
And Oxidative Stress

In sickle cell disease, nitric oxide (NO) depletion by cell-free plasma hemoglobin and/or oxygen radicals is associated with arginine deficiency, impaired NO bioavailability, and chronic oxidative stress. In transgenic-knockout sickle (BERK) mice that express exclusively human α- and βS-globins, reduced NO bioavailability is associated with induction of non-NO vasodilator enzyme, cyclooxygenase (COX)-2, and impaired NO-mediated vascular reactivity. We hypothesized that enhanced NO bioavailability in sickle mice will abate activity of non-NO vasodilators, improve vascular reactivity, decrease hemolysis, and reduce oxidative stress. Arginine treatment of BERK mice (5% arginine in mouse chow for 15 days) significantly reduced expression of non-NO vasodilators COX-2 and heme oxygenase-1. The decreased COX-2 expression resulted in reduced prostaglandin E2(PGE2) levels. The reduced expression of non-NO vasodilators was associated with significantly decreased arteriolar dilation and markedly improved NO-mediated vascular reactivity. Arginine markedly decreased hemolysis and oxidative stress and enhanced NO bioavailability. Importantly, arteriolar diameter response to a NO donor (sodium nitroprusside) was strongly correlated with hemolytic rate (and nitrotyrosine formation), suggesting that the improved microvascular function was a response to reduced hemolysis. These results provide a strong rationale for therapeutic use of arginine in sickle cell disease and other hemolytic diseases.

scholarly journals Nitric Oxide, Oxidative Stress, andp66ShcInterplay in Diabetic Endothelial Dysfunction

2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Alessandra Magenta ◽  
Simona Greco ◽  
Maurizio C. Capogrossi ◽  
Carlo Gaetano ◽  
Fabio Martelli
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Diabetic Patients ◽  
Oxygen Species ◽  
Complex Interplay ◽  
Cell Dysfunction ◽  
Intracellular Ros ◽  
No Bioavailability

Increased oxidative stress and reduced nitric oxide (NO) bioavailability play a causal role in endothelial cell dysfunction occurring in the vasculature of diabetic patients. In this review, we summarized the molecular mechanisms underpinning diabetic endothelial and vascular dysfunction. In particular, we focused our attention on the complex interplay existing among NO, reactive oxygen species (ROS), and one crucial regulator of intracellular ROS production,p66Shcprotein.

scholarly journals Study of the mechanisms of aldosterone prothrombotic effect in rats

2011 ◽  
Vol 12 (4) ◽  
pp. 430-439 ◽  
Author(s):  
Anna Gromotowicz ◽  
Janusz Szemraj ◽  
Adrian Stankiewicz ◽  
Agnieszka Zakrzeska ◽  
Maria Mantur ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Venous Thrombosis ◽  
Platelet Adhesion ◽  
Thrombus Formation ◽  
Mrna Levels ◽  
Stress Dependent ◽  
And Oxidative Stress ◽  
Pai 1

Introduction: We investigated the role of primary haemostasis, fibrinolysis, nitric oxide (NO) and oxidative stress as well as mineralocorticoid receptors (MR) in acute aldosterone prothrombotic action. Materials and methods: Venous thrombosis was induced by stasis in Wistar rats. Aldosterone (ALDO; 10, 30, 100 µg/kg/h) was infused for 1 h. Eplerenone (EPL; 100 mg/kg, p.o.), a selective MR antagonist, was administered before ALDO infusion. Bleeding time (BT) and platelet adhesion to collagen were evaluated. The expression of nitric oxide synthase (NOS), NADPH oxidase, superoxide dismutase (SOD) and plasminogen activator inhibitor (PAI-1) was measured. NO, malonyl dialdehyde (MDA) and hydrogen peroxide (H2O2) plasma levels were assayed. Results: Significant enhancement of venous thrombosis was observed after ALDO infusion. ALDO shortened BT and increased platelet adhesion. Marked increases were observed in PAI-1, NADPH oxidase and SOD mRNA levels. MDA and H2O2 levels were augmented in ALDO-treated groups, and NOS expression and NO level were decreased. EPL reduced ALDO effects on thrombus formation, primary haemostasis, PAI-1 expression and MDA level. Conclusion: Short-term ALDO infusion enhances experimental venous thrombosis in the mechanism involving primary haemostasis, fibrinolysis, NO and oxidative stress-dependent pathways. The MR antagonist only partially diminished the ALDO effects, suggesting the involvement of additional mechanisms.

Role of peroxynitrite in altered fetal-placental vascular reactivity in diabetes or preeclampsia

2000 ◽  
Vol 278 (4) ◽  
pp. H1311-H1319 ◽  
Author(s):  
Wilhelm Kossenjans ◽  
Annie Eis ◽  
Rashmi Sahay ◽  
Diane Brockman ◽  
Leslie Myatt
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Glyceryl Trinitrate ◽  
Human Placenta ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Ang Ii ◽  
Vascular Responses ◽  
Before And After

Oxidative stress may increase production of superoxide and nitric oxide, leading to formation of prooxidant peroxynitrite to cause vascular dysfunction. Having found nitrotyrosine residues, a marker of peroxynitrite action, in placental vessels of preeclamptic and diabetic pregnancies, we determined whether vasoreactivity is altered in these placentas and treatment with peroxynitrite produces vascular dysfunction. The responses of diabetic, preeclamptic, and normal placentas to increasing concentrations of the vasoconstrictors U-46619 (10− 9–10− 7M) and ANG II (10− 9–10− 7M) and the vasodilators glyceryl trinitrate (10− 9–10− 7M) and prostacyclin (PGI2; 10− 8–10− 6M) were compared as were responses to these agents in normal placentas before and after treatment with 3.16 × 10− 4 M peroxynitrite for 30 min. Responses to both vasoconstrictors and vasodilators were significantly attenuated in diabetic and preeclamptic placentas compared with controls. Similarly, responses to U-46619, nitroglycerin, and PGI2, but not ANG II, were significantly attenuated following peroxynitrite treatment. The presence of nitrotyrosine residues confirmed peroxynitrite interaction with placental vessels. Overall, our data suggest that peroxynitrite formation is capable of attenuating vascular responses in the human placenta.

scholarly journals Genetic Deletion of ACE2 Induces Vascular Dysfunction in C57BL/6 Mice: Role of Nitric Oxide Imbalance and Oxidative Stress

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0150255 ◽  
Author(s):  
Luiza A. Rabelo ◽  
Mihail Todiras ◽  
Valéria Nunes-Souza ◽  
Fatimunnisa Qadri ◽  
István András Szijártó ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Genetic Deletion ◽  
And Oxidative Stress

scholarly journals Oxidative stress is not associated with vascular dysfunction in a model of alloxan-induced diabetic rats

2010 ◽  
Vol 54 (6) ◽  
pp. 530-539 ◽  
Author(s):  
Verena Kise Capellini ◽  
Caroline Floreoto Baldo ◽  
Andréa Carla Celotto ◽  
Marcelo Eduardo Batalhão ◽  
Evelin Capellari Cárnio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Experimental Model ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Diabetic Rats ◽  
Nitrite Nitrate ◽  
Oxide Synthase ◽  
And Control ◽  
Inducible Nitric Oxide

OBJECTIVES: To verify if an experimental model of alloxan-diabetic rats promotes oxidative stress, reduces nitric oxide bioavailability and causes vascular dysfunction, and to evaluate the effect of N-acetylcysteine (NAC) on these parameters. METHODS: Alloxan-diabetic rats were treated or not with NAC for four weeks. Plasmatic levels of malondialdehyde (MDA) and nitrite/nitrate (NOx), the endothelial and inducible nitric oxide synthase (eNOS and iNOS) immunostaining and the vascular reactivity of aorta were compared among diabetic (D), treated diabetic (TD) and control (C) rats. RESULTS: MDA levels increased in D and TD. NOx levels did not differ among groups. Endothelial eNOS immunostaining reduced and adventitial iNOS increased in D and TD. The responsiveness of rings to acetylcholine, sodium nitroprusside, and phenylephrine did not differ among groups. CONCLUSIONS: NAC had no effect on the evaluated parameters and this experimental model did not promote vascular dysfunction despite the development of oxidative stress.

The sesame lignan sesamin attenuates vascular dysfunction in streptozotocin diabetic rats: Involvement of nitric oxide and oxidative stress

2013 ◽  
Vol 698 (1-3) ◽  
pp. 316-321 ◽  
Author(s):  
Tourandokht Baluchnejadmojarad ◽  
Mehrdad Roghani ◽  
Mohammad-Reza Jalali Nadoushan ◽  
Mohammad-Reza Vaez Mahdavi ◽  
Hamid Kalalian-Moghaddam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats ◽  
And Oxidative Stress

Procyanidins extracted from the litchi pericarp ameliorate atherosclerosis in ApoE knockout mice: their effects on nitric oxide bioavailability and oxidative stress

2017 ◽  
Vol 8 (11) ◽  
pp. 4210-4216 ◽  
Author(s):  
Shuang Rong ◽  
Xueting Hu ◽  
Siqi Zhao ◽  
Yanting Zhao ◽  
Xiao Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiovascular Diseases ◽  
Knockout Mice ◽  
Epidemiological Studies ◽  
Apoe Knockout Mice ◽  
And Oxidative Stress ◽  
Litchi Pericarp ◽  
Nitric Oxide Bioavailability

Epidemiological studies strongly support the role of procyanidin-rich beverages and fruit in the prevention of cardiovascular diseases.

scholarly journals Regulation of Inflammation and Oxidative Stress by Formyl Peptide Receptors in Cardiovascular Disease Progression

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 243
Author(s):  
Valentina Maria Caso ◽  
Valentina Manzo ◽  
Tiziana Pecchillo Cimmino ◽  
Valeria Conti ◽  
Pio Caso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Nadph Oxidase ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Ros Production ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Anti Inflammatory

G protein-coupled receptors (GPCRs) are the most important regulators of cardiac function and are commonly targeted for medical therapeutics. Formyl-Peptide Receptors (FPRs) are members of the GPCR superfamily and play an emerging role in cardiovascular pathologies. FPRs can modulate oxidative stress through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species (ROS) production whose dysregulation has been observed in different cardiovascular diseases. Therefore, many studies are focused on identifying molecular mechanisms of the regulation of ROS production. FPR1, FPR2 and FPR3 belong to the FPRs family and their stimulation triggers phosphorylation of intracellular signaling molecules and nonsignaling proteins that are required for NADPH oxidase activation. Some FPR agonists trigger inflammatory processes, while other ligands activate proresolving or anti-inflammatory pathways, depending on the nature of the ligands. In general, bacterial and mitochondrial formylated peptides activate a proinflammatory cell response through FPR1, while Annexin A1 and Lipoxin A4 are anti-inflammatory FPR2 ligands. FPR2 can also trigger a proinflammatory pathway and the switch between FPR2-mediated pro- and anti-inflammatory cell responses depends on conformational changes of the receptor upon ligand binding. Here we describe the detrimental or beneficial effects of the main FPR agonists and their potential role as new therapeutic and diagnostic targets in the progression of cardiovascular diseases.

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