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

Author(s):  
Areej Mohamed Ateya ◽  
Dr. Nagwa Ali Sabri ◽  
Dr. Ihab El Hakim ◽  
Dr. Sara M Shaheen

<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.

Medicine ◽  
2018 ◽  
Vol 97 (37) ◽  
pp. e11971 ◽  
Author(s):  
Yan Lu ◽  
Ren-gang Chen ◽  
San-zou Wei ◽  
Han-guo Hu ◽  
Fei Sun ◽  
...  

2012 ◽  
Vol 82 (1) ◽  
pp. 41-52 ◽  
Author(s):  
P. Earnest ◽  
S. Kupper ◽  
M. Thompson ◽  
Guo ◽  
S. Church

Homocysteine (HCY), C-reactive protein (hsCRP), and triglycerides (TG) are risk factors for cardiovascular disease (CVD). While multivitamins (MVit) may reduce HCY and hsCRP, omega-3 fatty acids (N3) reduce TG; yet, they are seldom studied simultaneously. We randomly assigned 100 participants with baseline HCY (> 8.0 umol/L) to the daily ingestion of: (1) placebo, (2) MVit (VitC: 200 mg; VitE: 400 IU; VitB6: 25 mg; Folic Acid: 400 ug; VitB12: 400 ug) + placebo, (3) N3 (2 g N3, 760 mg EPA, 440 mg DHA)+placebo, or (4) MVit + N3 for 12 weeks. At follow-up, we observed significant reductions in HCY (umol/L) for the MVit (- 1.43, 95 %CI, - 2.39, - 0.47) and MVit + N3 groups (- 1.01, 95 %CI, - 1.98, - 0.04) groups, both being significant (p < 0.05) vs. placebo (- 0.57, 95 %CI, - 1.49, 0.35) and N3 (1.11, 95 % CI, 0.07, 2.17). hsCRP (nmol/L) was significantly reduced in the MVit (- 6.00, 95 %CI, - 1.04, - 0.15) and MVit + N3 (- 0.98, 95 %CI, - 1.51, - 0.46) groups, but not vs. placebo (- 0.15, 95 %CI, - 0.74, 0.43) or N3 (- 0.53, 95 %CI, - 1.18, 0.12). Lastly, we observed significant reductions in TG for the N3 (- 0.41, 95 %CI, - 0.69, - 0.13) and MVit + N3 (- 0.71, 95 %CI, - 0.93, - 0.46) groups, both significant vs. placebo (- 0.10, 95 %CI, - 0.36, 0.17) and MVit groups (0.15, 95 %CI, - 12, 0.42). The co-ingestion of MVit + N3 provides synergistic affects on HCY, hsCRP, and plasma TG.


2021 ◽  
Author(s):  
Sankar Jamuna ◽  
Rathinavel Ashokkumar ◽  
Niranjali Devaraj Sivasithamparam

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.


2011 ◽  
Vol 6 (1) ◽  
pp. 14-17 ◽  
Author(s):  
Jay L. Myers ◽  
Jorie C. Allen

Evidence indicates that chronic diseases, such as cardiovascular disease, obesity, and asthma are part of a group of conditions linked by inflammatory dysregulation. One explanation for these associations is that the Western diet is obeseogenic and promotes the secretion of inflammatory biochemical signals. Weight gain results in lipid accumulation and adipocyte stress—factors known to disrupt the balance of systemic cell signaling (adipokines and cytokines) that favors inflammation. Markers are used as indicators of the inflammatory milieu and include the measurement of proinflammatory (C-reactive protein, interleukin-6, tumor necrosis factor-a) and anti-inflammatory (adiponectin) signaling molecules. Consumption of a high ratio of omega-6 to omega-3 fatty acids is also an important indicator for a potentially inflammatory profile. This ratio may determine the direction of biological pathways for another family of inflammatory mediators—eicosanoids—which vary according to the omega fatty acid precursor. An improved dietary pattern that emphasizes balanced energy and nutrient intake resulting in a reduced ratio of omega-6 to omega-3 fatty acids plays a particularly important role in inflammation management.


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