scholarly journals Polyphenols in preventing endothelial dysfunction

2017 ◽  
Vol 71 (1) ◽  
pp. 0-0 ◽  
Author(s):  
Sylwia Biegańska-Hensoldt ◽  
Danuta Rosołowska-Huszcz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Oxidative Dna Damage ◽  
Developed Countries ◽  
The Body ◽  
No Production ◽  
C Reactive Protein ◽  
Rat Cardiomyocytes ◽  
Reactive Protein

One of the main causes of mortality in developed countries is atherosclerosis. The pathogenesis of atherosclerosis is associated with endothelial dysfunction. Consumption of food rich in natural antioxidants including polyphenols significantly improves endothelial cells functions.Polyphenols have a beneficial effect on the human body and play an important part in protecting the cardiovascular system. Polyphenols present in food have antioxidant, anti-inflammatory, antihypertensive, antithrombotic and antiproliferative properties. Catechins cause an increase in the activity of endothelial nitric oxide synthase (eNOS) and increased production of nitric oxide (NO) and decrease in blood pressure. Catechins also reduce platelet adhesion, lower the concentration of C-reactive protein and tumor necrosis factor alpha and interleukin-6. Resveratrol inhibits NADPH oxidase expression, increases the expression of eNOS and NO production as well as decreases the expression of proinflammatory cytokines, and also lowers the concentration of the soluble forms of adhesion molecules – sICAM-1 and sVCAM-1 in blood. Quercetin reduces the blood level of low density lipoprotein cholesterol, lowers blood pressure, reduces the concentration of C-reactive protein and F2-isoprostane level. Curcumin has antagonistic activity to homocysteine. Curcumin increases the expression of eNOS and reduces oxidative DNA damage in rat cardiomyocytes. Numerous attempts are taken for improving the bioavailability of polyphenols in order to increase their use in the body.

scholarly journals Amelioration of C - Reactive Protein and Lectin Like Oxidised Low Density Lipoprotein Receptor Complex Induced Endothelial Dysfunction by Oligomeric Proanthocyanidins.

2021 ◽  
Author(s):  
Sankar Jamuna ◽  
Rathinavel Ashokkumar ◽  
Niranjali Devaraj Sivasithamparam
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Capillary Tube ◽  
Morphological Changes ◽  
Protein Docking ◽  
Pcr Analysis ◽  
Inhibitory Mechanism ◽  
C Reactive Protein ◽  
Reactive Protein

Abstract C-reactive protein (CRP) is a well established biochemical marker for atherosclerosis. Inflammation induced by CRP promotes endothelial dysfunction. Modification of LDL inside the artery wall favors the elevation of this acute phase protein. The mechanism of OxLDL+CRP complex is unrevealed so far. Hence, this mechanism was considered as the important factor to trigger the monocyte to macrophages differentiation which in leads to foam cells formation. Hence this key event should be targeted and focused on how this complex (OxLDL+CRP) proceeds to endothelial dysfunction. OPC is a well known cardioprotective flavon-3-ols. The present study is challenged between the protective roles of OPC against the deleterious effect of this complex (OxLDL+CRP) on endothelial cells. Monolayer of Endothelial cells were incubated with THP-1 monocytes for 48 h supplemented with OxLDL (10mg/ml) + CRP (10 mg/ml) complex and treated with OPC (100mg/ml). Morphological changes, cell migration assay and capillary tube forming assay was carried out. Myeleoperoxidase levels were estimated to determine the adhesion of monocytes onto EC monolayer. RT-PCR analysis of L-Selectin was done. The quantification of NO levels and analysis of mRNA expressions of eNOS is to determine the nitric oxide demand caused due to OxLDL+CRP complex. LOX-1, scavenger receptor levels were analysed by mRNA expression. Proinflammatory markers such as IL-6, MCP-1 and IL-1b were studied. Accumulation of ROS levels were measured fluorimetrically using DCF-DA. Spectrophotometric analysis of Sirius red dye binding collagen levels was observed. Mitochondrial membrane potential was determined by JC-1 dye and cell cycle analysis was done by FACS analysis. Protein –Protein docking was carried out between CRP and LOX-1. This docked protein complex were again docked with OPC and atrovastatin to show the inhibitory mechanism of CRP binding with LOX-1. OPC showed a promising inhibitory mechanism against OxLDL+CRP complex. To emphasis the results OPC treated group showed decreased levels of proinflammatory markers, LOX-1 and L-Selectin levels. Endothelial nitric oxide levels were increased upon OPC treatment and reduction in the ROS levels. Endothelial cells apoptosis was prevented by OPC. Docking studies showed that in the absence of ligands (OPC) binding of CRP and LOX-1 was greater and vice versa in the presence of ligands. To conclude, OxLDL + CRP complex inhibitory effects of OPC could maintain the normal homeostasis.

scholarly journals Effect of Cadmium Exposure in Polymorphisms Gene NOS3, Blood Cadmium Level, Nitric Oxide Level, Blood Pressure and Antioxidant Enzymes

2018 ◽  
Vol 73 ◽  
pp. 06006
Author(s):  
Hernayanti ◽  
Santoso Slamet ◽  
Lestari Sri
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Antioxidant Enzyme ◽  
Human Life ◽  
The Body ◽  
No Production ◽  
Textile Materials ◽  
Length Polymorphisms ◽  
Exposed Individual ◽  
Result Show

Cadmium is one of a heavy metal which widely used in human life, especially in the electroplating industry and a mixture of textile materials. Cadmium that enters the body binds to the metallothioneins protein. It can increase the formation of free radical compounds, there by inhibiting enzyme activity such as nitric oxide synthase3. This gene regulates the expression of endothelial nitric oxide synthase which produce a nitric oxide. Nitric oxide role in regulated blood pressure as vasodilator with Angiotensin II as vasoconstriction. The susceptibility to Cd exposure will elevate if the polymorphisms of gene is found in population. The aim of this research was to know effect of cadmium to gene NOS3 polymorphisms on NO, systolic and diastolic blood pressure and antioxidant enzyme in Cd-exposed individual. The genotype individual were detected by Polymerase Chain Reaction-Restriction Fragment Length Polymorphisms (PCR-RLFP) with MBo1 restriction enzyme. Parameter recorded were blood Cd , NO level, SOD, systolic and diastolic. Data were analyzed by independent t-test. These result showed that 20% of 40 individual of cases subject were detected as polymorphisms individual of NOS3gene, with GA genotype. Their fragment DNA located on 206 bp, 119 bp and 87 bp, but non polymorphisms of NO gene is only located on 206 bp. The result show cadmium could influence polymorphisms NOS3gene and decrease NO production followed by increasing of blood pressure both systolic and diastolic. Cadmium also decrease antioxidant enzyme SOD and GPx level.

scholarly journals Does omega-3 fatty acids supplementation affect C-Reactive protein and Nitric oxide in pediatric patients undergoing hemodialysis?

2016 ◽  
Vol 5 (5) ◽  
Author(s):  
Areej Mohamed Ateya ◽  
Dr. Nagwa Ali Sabri ◽  
Dr. Ihab El Hakim ◽  
Dr. Sara M Shaheen
Keyword(s):  
Nitric Oxide ◽  
Fatty Acids ◽  
Endothelial Dysfunction ◽  
Pediatric Patients ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
C Reactive Protein ◽  
Once Daily ◽  
Reactive Protein ◽  
Traditional Risk Factors

<italic>Background:</italic>Chronic kidney disease (CKD) is a worldwide public health problem in the pediatric population. Patients with CKD die of cardiovascular causes rather than from renal disease. There are several traditional and non-traditional risk factors for cardiovascular disease (CVD) in these patients. Endothelial dysfunction is one of the non-traditional risk factors for CVD. Many studies have shown the ability of omega-3 fatty acids to improve the endothelial function and reduce the cardiovascular events in the general population. Thus, the aim of this study was to evaluate the effect of omega-3 fatty acids supplementation on markers of endothelial dysfunction in children with CKD on regular hemodialysis (HD). <italic>Methods and procedures:</italic> This double-blinded randomized placebo-controlled trial included 49 pediatric patients on maintenance HD. Group 1 (n=25) received 1 g omega-3 capsule once daily and group 2 (n=24) received 1 g matched placebo capsule once daily. Both groups were treated for four months. Blood samples were taken from patients of both groups at baseline and after 4 months of supplementation. Serum samples were examined for C-reactive protein (CRP) and nitric oxide (NO) levels as markers of endothelial dysfunction. <italic>Results:</italic> Our results showed that CRP was reduced insignificantly in omega-3 group. NO levels showed no significant differences between groups at the end of the study. <italic>Conclusion:</italic> The administration of 1 g omega-3 capsule once daily for 4 months had no beneficial effects neither on CRP nor NO but should evaluate more.

scholarly journals The effects of renal replacement therapy on plasma, asymmetric dimethylarginine, nitric oxide and C-reactive protein levels

2008 ◽  
Vol 31 (1) ◽  
pp. 1 ◽  
Author(s):  
Halfize Uzun ◽  
Dildar Konukoglu ◽  
Mine Besler ◽  
Fusun Erdenen ◽  
Can Sezgin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Renal Replacement Therapy ◽  
Endothelial Dysfunction ◽  
Replacement Therapy ◽  
Asymmetric Dimethylarginine ◽  
C Reactive Protein ◽  
Plasma Urea ◽  
Reactive Protein ◽  
Plasma Adma

Purpose: Asymmetric dimethylarginine (ADMA), nitric oxide (NOx), and C-reactive protein (CRP) are important risk factors for endothelial dysfunction and mortality in the end stage renal diseases population. The aim of the study was to investigate the relationship between renal replacement therapy and endothelial dysfunction. Methods: Plasma NOx, ADMA and CRP levels were examined in randomized selected 30 patients with chronic kidney diseases (CKD), 28 patients receiving continuous ambulatory peritoneal dialysis (PD) and 30 patients receiving regular hemodialysis (HD) and age-matched 20 healthy controls. The duration of dialysis was from 4, 5 to 11, and 6 years, respectively. Results: CKD patients had higher plasma ADMA (1.26±0.53?mol/L) and CRP levels (1.02±025mg/L) and lower NOx levels (28.6±5.4?mol/L) than controls (0.45±0.20; 0.65± 0.45; 32.5±37 respectively, P < 0.001).Plasma NOx and CRP levels were higher in HD patients (32.9±5.5?mol/L, P < 0.05 and 4.59±3.18mg/L, P < 0.001) and plasma ADMA and CRP levels were higher in PD patients (1.82±0.98?mol/L, P < 0.001 and 2.40±1.53mg/L, P < 0.001) than in CKD patients. PD patients had higher plasma ADMA levels (P < 0.05) and lower plasma NOx and CRP levels than HD patients (P < 0.001 and P < 0.001). Plasma ADMA levels were negatively correlated with NOx levels in all patient groups (P < 0.001). Plasma CRP levels in CKD and HD patients were positively correlated with plasma urea levels (r:0,437, P < 0,001) and duration of dialysis (r:0,370, P < 0.01), respectively. Conclusion: CRP and ADMA may be emerging as important risk factors for atherosclerosis in dialysis patients. Reduced NO elaboration secondary to accumulation of ADMA and elevated inflammation may be important pathogenic factors for endothelial dysfunction in both dialysis treatment strategies.

scholarly journals MARKERS OF ENDOTHELIAL DYSFUNCTION: PATHOGENETIC ROLE AND DIAGNOSTIC SIGNIFICANCE

2019 ◽  
Vol 64 (1) ◽  
pp. 34-41 ◽  
Author(s):  
T. V. Stepanova ◽  
A. N. Ivanov ◽  
N. E. Tereshkina ◽  
E. B. Popyhova ◽  
D. D. Lagutina
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Asymmetric Dimethylarginine ◽  
Vascular Endothelial ◽  
C Reactive Protein ◽  
Pathogenetic Role ◽  
Reactive Protein ◽  
Von Willebrand ◽  
Endothelial Growth Factor ◽  
Willebrand Factor

Endothelial dysfunction (ED) is considered one of the pathogenetic mechanisms of a whole range of diseases. Detection of specific biochemical markers in the blood is an effective way to ED diagnostics that characterize the vascular endothelium state. This review highlights the pathogenetic role of the factors synthesized by endotheliocytes whose level changes in biological fluids reflect violations of the endothelium basic physiological properties: vasomotor function, thromboresistance, angiogenesis regulation, barrier and adhesion functions. In particular, the participation of nitric oxide metabolites, asymmetric dimethylarginine, endothelin-1, metabolic products of arachidonic acid, von Willebrand factor, thrombomodulin, vascular endothelial growth factor, vasohibine-1 and adhesion molecules in the onset and development of ED are reviewed. The diagnostic significances of factors damaging endothelium, such as C-reactive protein, homocysteine and 8-hydroxy-2’-deoxyguanosine, are discussed. In addition, the literature data of recent years about the prospects of clinical implication the detection of the above-mentioned factors which indicates structural and functional endothelial cells damage are given. Particular attention is paid to the ED markers detection prognostic significance and the possibility of their practical use for the ED diagnosis. The search of literature for the current review was conducted in RSIC, CyberLeninka, Scopus, Web of Science, MedLine and PubMed databases from 2012 to 2018 using the following keywords: endothelial dysfunction, nitric oxide, asymmetric dimethylarginine, endothelin-1, prostacyclin, thromboxane A2, epoxyeicosatrienoic acids, von Willebrand factor, thrombomodulin, vascular endothelial growth factor, vasohibin-1, adhesive molecules, C-reactive protein, homocysteine, and 8-hydroxy-2-deoxyguanosine.

scholarly journals Biomarkers of endothelial dysfunction in cardiovascular diseases

2017 ◽  
Vol 70 (1-2) ◽  
pp. 53-57
Author(s):  
Sonja Smiljic ◽  
Milica Mijovic ◽  
Sladjana Savic
Keyword(s):  
Nitric Oxide ◽  
Extracellular Matrix ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Dysfunction ◽  
Adhesion Molecules ◽  
Vascular Endothelial ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Endothelial Growth Factor

Introduction. Endothelial dysfunction is the result of numerous infectious or noninfectious acute and chronic diseases, mechanical damage, hemodynamic imbalance and effects of certain drugs. Endothelial dysfunction can be assessed by determining biomarkers (adhesion molecules, inflammatory cytokines and growth factors, and noninvasive visualization biomarkers). Intercellular adhesion molecule-1 and vascular cellular adhesion molecule. Adhesion molecules mediate the interaction of cells with the extracellular matrix, as well as with other cells. It is shown that adhesion molecules and molecules of the extracellular matrix are markers of endothelial dysfunction and they are involved in the pathogenesis of atherosclerosis. P-selectin and E-selectin. Determination of these two mediators is important not only in the evaluation of endothelial damage in acute inflammation, but in other chronic non-infectious conditions such as atherosclerosis. C-reactive protein. C-reactive protein reduces the transcription of endothelial nitric oxide synthase at the level of the endothelial cells and ?destabilize? their messenger ribonucleic acid, thus leading to a reduction of the synthesis of nitric oxide, in the basal and stimulated conditions, which is significant for the development of endothelial dysfunction as a part of the formation of subclinical atherosclerosis. Vascular endothelial growth factor, fibrinogen and thrombomodulin. Vascular endothelial growth factor is a cytokine that stimulates angiogenesis for the purpose of revascularization of ischemic tissues, and mediates in a variety of functions of endothelial cells, including proliferation, migration, invasion, survival and permeability. Noninvasive visualization biomarkers. Determination of intima-media complex thickness and calcium score index by computed tomography are considered clinically reliable methods in prevention and early diagnosis of coronary artery disease and acute myocardial infarction, changing the basic concepts of prevention. Conclusion. At this point it is not easy to say what clinical significance are listed biomarkers of endothelial dysfunction in determining the risk for cardiovascular disease.

scholarly journals C-reactive protein and its relation to high blood pressure in overweight or obese children and adolescents

2013 ◽  
Vol 31 (3) ◽  
pp. 331-337 ◽  
Author(s):  
Juliana Andreia F. Noronha ◽  
Carla Campos M. Medeiros ◽  
Anajás da Silva Cardoso ◽  
Nathalia Costa Gonzaga ◽  
Alessandra Teixeira Ramos ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Children And Adolescents ◽  
High Blood Pressure ◽  
Severe Obesity ◽  
The Body ◽  
Obese Children ◽  
C Reactive Protein ◽  
Cross Sectional ◽  
Reactive Protein ◽  
Hs Crp

OBJECTIVE To investigate the association between C-reactive protein (CRP) and high blood pressure (BP) in overweight or obese children and adolescents. METHODS Cross-sectional study with 184 overweight or obese children and adolescents aged from two to 18 years old, from April, 2009 to April, 2010. The classification of nutritional status used the body mass index (BMI). Based on the Centers for Disease Control and Prevention curve, individuals were classified as: overweight (BMI between the 85th-95th percentiles), obesity (BMI between 95th-97th percentiles) and severe obesity (BMI >97th percentile). Abnormal values were considered for systolic BP (SBP) and/or diastolic (DBP) if ≥90th percentile of the BP curve recommended for children and adolescents in the V Brazilian Guidelines on Hypertension, for waist circumference (WC) if ≥90th percentile of the curve established by the National Cholesterol Education Program, and for high sensitive CRP (hs-CRP) if >3mg/dL. To evaluate the association of inadequate values of CRP and the studied groups, chi-square test and analysis of variance were applied, using the Statistical Package for the Social Sciences version 17.0 and adopting a significance level of 5%. RESULTS Among the evaluated sample, 66.3% were female, 63.5%, non-white, 64.1% had severe obesity, 78.3% had altered WC and 70.6% presented high BP. There was a significant association of CRP high levels with altered WC and BMI ≥97th percentile. In adolescents, high CRP was related to high SBP. CRP mean values were higher in individuals with elevated SBP. CONCLUSIONS Inadequate values of hs-CRP were associated with severe obesity and high SBP in the studied population. These markers can be used to identify children and adolescents at higher risk for developing atherosclerosis.

scholarly journals Clinically relevant high levels of human C-reactive protein induces endothelial dysfunction and hypertension by inhibiting the AMPK-eNOS axis

2020 ◽  
Vol 134 (13) ◽  
pp. 1805-1819
Author(s):  
Lele Cheng ◽  
Liang Wang ◽  
Manyun Guo ◽  
Jinlong He ◽  
Yangyang Deng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
C Reactive Protein ◽  
Inflammatory Biomarker ◽  
Reactive Protein ◽  
Enos Phosphorylation ◽  
Potential Strategy ◽  
High Level ◽  
Amp Activated Protein Kinase ◽  
Endothelial Nitric Oxide

Abstract Successful treatment of resistant hypertension accompanied by elevated human C-reactive protein (hCRP) remains a key challenge in reducing the burden of cardiovascular diseases. It is still unclear whether clinically relevant high-level hCRP is merely a marker or a key driver of hypertension. Here, we investigated the role and mechanism of clinically relevant high level of hCRP in hypertension. Elevated blood pressure was observed in all three hCRP overexpression models, including adeno-associated virus 9 (AAV9)-transfected mice, AAV9-transfected rats and hCRP transgenic (hCRPtg) rats. hCRPtg rats expressing clinically relevant high-level hCRP developed spontaneous hypertension, cardiac hypertrophy, myocardial fibrosis and impaired endothelium-dependent relaxation. Mechanistically, studies in endothelial nitric oxide (NO) synthase (eNOS) knockout mice transfected with AAV9-hCRP and phosphoproteomics analysis of hCRP-treated endothelial cells revealed that hCRP inhibited AMP-activated protein kinase (AMPK)-eNOS phosphorylation pathway. Further, activation of AMPK by metformin normalized endothelial-dependent vasodilation and decreased the blood pressure of hCRPtg rats. Our results show that clinically relevant high-level hCRP induces hypertension and endothelial dysfunction by inhibiting AMPK-eNOS signaling, and highlight hCRP is not only an inflammatory biomarker but also a driver of hypertension. Treatment with metformin or a synthetic AMPK activator may be a potential strategy for vaso-dysfunction and hypertension in patients with high hCRP levels.

scholarly journals Adeno-Associated Virus–Mediated Human C-Reactive Protein Gene Delivery Causes Endothelial Dysfunction and Hypertension in Rats

2009 ◽  
Vol 55 (2) ◽  
pp. 274-284 ◽  
Author(s):  
Hongjing Guan ◽  
Peihua Wang ◽  
Rutai Hui ◽  
Matthew L Edin ◽  
Darryl C Zeldin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fluorescent Protein ◽  
Left Ventricular ◽  
Maximum Pressure ◽  
No Production ◽  
C Reactive Protein ◽  
Adeno Associated Virus ◽  
Reactive Protein ◽  
Angiotensin Type 2 Receptor ◽  
Angiotensin Type

Abstract Background: Prospective studies have shown that C-reactive protein (CRP) is a predictor of hypertension. Because of confounding variables, a causal linkage between CRP and hypertension has not been clearly shown. We investigated whether high circulating concentrations of human CRP can induce hypertension in rats. Methods: We administered a single intravenous injection of adeno-associated virus–green fluorescent protein (AAV-GFP) or AAV-hCRP and measured blood pressure. Using ELISA, we measured serum hCRP, serum endothelin 1 (ET-1), and urine cGMP, and we measured serum nitric oxide (NO) using the Griess method. We recorded heart rate, maximum pressure, arterial elastance, mean aortic pressure, cardiac output, and maximum rate of rise in left ventricular pressure (dP/dt max). Results: A single injection of AAV-hCRP resulted in efficient and sustained hCRP expression and led to increased blood pressure 2 months after gene transfer that persisted for another 2 months. This effect was associated with decreased NO production, as demonstrated by decreased serum NO concentration and urinary cGMP excretion, and impairment of endothelial-dependent vascular relaxation. CRP transduction also increased expression of angiotensin type 1 receptor, ET-1, and endothelin type A receptor, decreased expression of angiotensin type 2 receptor and endothelial NO synthase in thoracic aortas, and increased arterial stiffness. Ex vivo studies indicated a similar detrimental effect of CRP that was reversed by the NO donor. Conclusion: AAV vector–mediated CRP expression resulted in hypertension mediated through reduced NO production and subsequent alteration in ET-1 and renin-angiotensin system activation. Impaired arterial elasticity may also contribute to CRP-induced hypertension. These results support a causal role for CRP in the pathogenesis of hypertension.

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