scholarly journals C-reactive protein impairs the endothelial glycocalyx resulting in endothelial dysfunction

2009 ◽  
Vol 84 (3) ◽  
pp. 479-484 ◽  
Author(s):  
S. Devaraj ◽  
J.-M. Yun ◽  
G. Adamson ◽  
J. Galvez ◽  
I. Jialal
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Glycocalyx ◽  
C Reactive Protein ◽  
Reactive Protein

P4679Changes in systemic inflammation and endothelial dysfunction after balloon pulmonary angioplasty

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
W Magon ◽  
J Stepniewski ◽  
K Jonas ◽  
M Waligora ◽  
P Podolec ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Serum Concentration ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
C Reactive Protein ◽  
Pulmonary Hemodynamics ◽  
Endothelin 1 ◽  
Reactive Protein ◽  
Balloon Pulmonary Angioplasty

Abstract Introduction Pulmonary endarterectomy leads to a decrease in systemic inflammation and improvement in endothelial function in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Balloon pulmonary angioplasty (BPA) improves pulmonary hemodynamics in patients with inoperable CTEPH. Aim To assess changes in systemic inflammation and endothelial dysfunction after a single BPA session and after completion of the treatment. Methods We enrolled consecutive, inoperable CTEPH patients who underwent BPA. Interleukin 6, 10 (IL-6, IL-10), and C-reactive protein (hsCRP) constituted markers of systemic inflammation. Endothelin-1 (ET-1) served as a marker of endothelial dysfunction. Serum concentration of selected markers was assessed in every patient before, 24 hours after the first BPA session and 6 months after completion of the BPA treatment. Age- and sex-matched healthy subjects served as a control group. Results We recruited 20 patients with inoperable CTEPH (6 males [30%]), aged 67 [61–74] years in New York Heart Association class III (n=19 [95%]) and II (n=1 [5%]). BPA treatment was completed with a median of 5 [2–8] BPA sessions per patient. Before starting the treatment CTEPH patients, as compared to controls (n=10), had raised serum level of IL-6 (3.82 [2.75 - 6.03] vs. 2.64 [0.88 - 4.75] pg/ml; p=0.04), hsCRP (2.47 [0.93 - 4.27] vs. 1.23 [0.48–3.21] ng/ml; p=0.02) and ET-1 (2.68 [2.24 - 3.64] vs. 1.47 [1.4 - 1.82] pg/ml; p=0.004). There was no difference in IL-10 level. 24 hours after a BPA session we observed an increased level of IL-6, IL-10 and hsCRP. (Tab.) 6 months after completion of the BPA treatment there was a reduced level of IL-6, hsCRP and ET-1 (Tab.) Table 1. Changes (Δ) in serum concentration of analyzed markers 24 hours after a single BPA session and at 6-months assessment after completion of the BPA treatment (n=20) Initial Δ at 24 hours after single BPA p Δ at 6-months follow-up p ET-1 [pg/ml] 2.68 [2.24; 3.64] −0.2 [−0.5; 0.23] 0.21 −0.47 [−0.96; 0.05] 0.004 IL-6 [pg/ml] 3.82 [2.75; 6.03] 3.67 [1.41; 7.16] 0.008 −0.82 [−3.11; 0.54] 0.04 IL-10 [pg/ml] 0.53 [0.44; 0.58] 0.32 [0.21; 0.87] 0.006 −0.11 [−0.33; 0.14] 0.94 hsCRP [ng/ml] 2.47 [0.93; 4.27] 5.4 [3.96; 10.59] 0.008 −0.36 [−0.94; 0.16] 0.02 ET-1, endothelin 1; hsCRP, C-reactive protein; IL-6, interleukin 6; IL-10, interleukin 10. Conclusions Patients with inoperable CTEPH, as compared to healthy controls, exhibit an increased systemic inflammation and endothelial dysfunction, which both improve after completion of the BPA treatment. At short-term follow-up after single BPA session there is an increase in systemic inflammatory response.

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.

Vitamin D Treatment Effect on Serum Endocan and High-Sensitivity C-Reactive Protein Levels in Renal Transplant Patients

2016 ◽  
Vol 26 (4) ◽  
pp. 335-339 ◽  
Author(s):  
Omer Atis ◽  
Mustafa Keles ◽  
Erdem Cankaya ◽  
Hasan Dogan ◽  
Hulya Aksoy ◽  
...  
Keyword(s):  
Vitamin D ◽  
Endothelial Dysfunction ◽  
Renal Transplant ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Transplant Patients ◽  
Vitamin D Levels ◽  
Hs Crp ◽  
25 Oh Vitamin D

Context: Endocan is a marker showing endothelial dysfunction and inflammation. Significantly increased endocan levels have been observed in serum of patients with sepsis and cancer. Objective: Our aim was to investigate the relationship between vitamin D treatment and serum endocan and high-sensitivity C-reactive protein (hs-CRP) levels as inflammatory markers in transplant patients. Design: Prospective. Setting: Nephrology clinic. Patients: Thirty-eight renal transplant patients with serum 25-hydroxy-vitamin D (25-OH-vitamin D) levels below 20 ng/mL and transplanted at least 12 months. Intervention: One-time oral dose of 300 000 IU vitamin D3. Main Outcome Measures: Before and after vitamin D treatment, serum endocan, hs-CRP, calcium, phosphorus, and parathyroid hormone (PTH) levels were measured. Results: Median serum endocan and PTH values before vitamin D were significantly higher than those of after treatment values ( P = .001 and P < .001, respectively). On the other hand, serum total calcium and phosphorus levels before vitamin D treatment were lower than the values obtained after vitamin D treatment ( P = .0013 and P < .001, respectively). Serum hs-CRP was lower after vitamin D therapy than before, but the difference was not statistically significant ( P = .06). A moderate negative correlation was determined between endocan and 25-OH-vitamin D levels after treatment with vitamin D ( r = −.36, P = .02). Conclusion: This study has revealed that vitamin D treatment reduced markers of endothelial dysfunction in patients with renal transplantation and vitamin D deficiency.

scholarly journals Endothelial dysfunction and C‐reactive protein predict the incidence of heart failure in hypertensive patients

2020 ◽  
Author(s):  
Raffaele Maio ◽  
Maria Perticone ◽  
Edoardo Suraci ◽  
Angela Sciacqua ◽  
Giorgio Sesti ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Dysfunction ◽  
C Reactive Protein ◽  
Hypertensive Patients ◽  
Reactive Protein

scholarly journals Insulin Resistance and High Sensitivity C-Reactive Protein in Migraine

2008 ◽  
Vol 35 (4) ◽  
pp. 448-451 ◽  
Author(s):  
Baburhan Guldiken ◽  
Sibel Guldiken ◽  
Muzaffer Demir ◽  
Nilda Turgut ◽  
Levent Kabayel ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
High Sensitivity ◽  
Analysis Of Covariance ◽  
Model Assessment ◽  
C Reactive Protein ◽  
Insulin Metabolism ◽  
Reactive Protein ◽  
Healthy Control ◽  
Hs Crp

Background:A relationship between migraine and vascular disorders such as hypertension, stroke, and coronary ischemia has been recently reported. Insulin resistance and endothelial dysfunction, which commonly underlies these disorders, have not been widely investigated in migraine patients. In this study, we aimed to investigate the existence of insulin resistance and endothelial dysfunction, and their relationship to vascular risk factors in patients with migraine.Methods:We evaluated insulin resistance and high-sensitivity C-reactive protein (hs-CRP), a marker of endothelial dysfunction, in 60 migraine patients and 25 healthy control subjects. Multiple analysis of covariance test was used to adjust for known confounding factors that can influence insulin metabolism and endothelial function, such as obesity, blood pressure, and lipid parameters.Results:Insulin resistance, as measured homeostasis model assessment (HOMA)-R levels, was significantly higher in the migraine group (p<0.001). After adjustment for confounding variables, the relationship between migraine and the HOMA-R levels remained significant (p<0.001). The hs-CRP levels did not differ between the migraine and control groups.Conclusions:Our data show that insulin resistance is present in migraine patients. Endothelial dysfunction is not found during the headache-free period. Further studies are needed to explain the role of insulin resistance in migraine pathogenesis.

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