scholarly journals The Influence of Sevelamer Hydrochloride and Calcium Carbonate on Markers of Inflammation and Oxidative Stress in Hemodialysis at Six Months of Follow-Up

2021 ◽  
Vol 8 ◽  
Author(s):  
Elodia Nataly Díaz-De la Cruz ◽  
José Ignacio Cerrillos-Gutiérrez ◽  
Andrés García-Sánchez ◽  
Carlos Gerardo Prado-Nevárez ◽  
Jorge Andrade-Sierra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Calcium Carbonate ◽  
Inflammatory Cytokines ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Sevelamer Hydrochloride ◽  
Tnf Α ◽  
Compensatory Effect ◽  
Pro Inflammatory Cytokines

Patients with end-stage renal disease (ESRD) present alterations in mineral and bone metabolism. Hyperphosphatemia in ESRD is considered an independent risk factor for cardiovascular disease (CVD), increasing morbidity, and mortality. Sevelamer hydrochloride is a calcium-free, non-absorbable phosphate-chelating polymer. Calcium carbonate chelator is helpful in controlling serum phosphate levels. There is insufficient information on the influence of sevelamer hydrochloride and calcium carbonate on the behavior of oxidative stress (OS) markers and inflammation in patients on hemodialysis (HD). A randomized open clinical trial was carried out on patients to evaluate sevelamer hydrochloride and calcium carbonate influence at 6 months of study follow-up. Levels of oxidants (LPO, NO, and 8-isoprostanes), antioxidants (SOD and TAC), oxidative DNA damage (8-OHdG and hOGG1), pro-inflammatory cytokines (IL-6 and TNF-α), and inflammation markers (ferritin and C-reactive protein) were measured with colorimetric and ELISA methods. We found a significant increase in oxidants LPO and NO, and antioxidants SOD and TAC, and downregulation of IL-6 and TNF-α. Ferritin decrease at 6 months follow-up in the sevelamer hydrochloride group. Increase in C-reactive protein was found in the group of patients treated with calcium carbonate. In conclusion, we found an oxidative state imbalance with increase in LPO and NO oxidants. The activity of the antioxidant enzymes (SOD and TAC) was also found to increase, suggesting a compensatory effect in the face of increase in oxidants. The same phenomenon was observed with increase in the oxidative damage marker to DNA and the increase in the DNA repair enzyme, suggesting a compensatory effect. Pro-inflammatory cytokines were predominantly downregulated by TNF-α in the group that ingested sevelamer hydrochloride in the final determination at 6 months of follow-up. Serum ferritin levels decreased significantly at the end of follow-up in patients on HD in the sevelamer hydrochloride group. The management of hyperphosphatemia with sevelamer hydrochloride appears to have obvious anti-inflammatory and antioxidant benefits.

scholarly journals Expression of proinflammatory cytokines in stable angina

2013 ◽  
Vol 4 (1) ◽  
pp. 20-23
Author(s):  
A. N Zakirova ◽  
N. E Zakirova
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Functional Class ◽  
Control Group ◽  
Moderate Increase ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Healthy Persons ◽  
Pro Inflammatory Cytokines

Objective: to evaluate the severity of immuno-inflammatory responses under stable stenocardia in patients with ischemic heart disease (IHD). Patients and intervention: the study included 83 patients suffering from IHD. Among them 30 cases were diagnosed as functional class (FC)-II stenocardia, 27 cases as FC-III stenocardia and 26 cases as FC-IV stenocardia. The control group included 25 healthy persons. For characterizing the immuno-inflammatory responses we examined the level of C-reactive protein (CRP), pro-inflammatory (IL-1b, IL-6, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokines by the immunoenzymic procedure. Results: FC-II stenocardia showed normal levels of CRP and pro-inflammatory cytokines. FC-III stenocardia was associated with a moderate increase in markers of an inflammation. FC-IV stenocardia was characterized by maximum levels of CRP and pro-inflammatory cytokines. Conclusion. The intensity of immuno-inflammatory responses depends on more or less serious course of stenocardia in patients with IHD.

scholarly journals Experimental Evaluation of the Impact of Gadolinium Orthovanadate GdVO4:Eu3+ Nanoparticles on the Carrageenan-Induced Intestinal Inflammation

2020 ◽  
Vol 63 (1) ◽  
pp. 18-24
Author(s):  
Anton S. Tkachenko ◽  
Galina I. Gubina-Vakulyck ◽  
Vladimir K. Klochkov ◽  
Nataliya S. Kavok ◽  
Anatolii I. Onishchenko ◽  
...  
Keyword(s):  
Blood Serum ◽  
Intestinal Inflammation ◽  
Intestinal Morphology ◽  
Oral Exposure ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Small Intestinal ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Aim: To evaluate the effects of orally administered gadolinium orthovanadate GdVO4:Eu3+ nanoparticles (VNPs) on the course of chronic carrageenan-induced intestinal inflammation. Methods: Samples of small intestinal tissue were collected from four groups of rats (intact, after administration of VNPs, with carrageenaninduced intestinal inflammation, with carrageenan-induced intestinal inflammation orally exposed to VNPs) to assess the intestinal morphology and HSP90α expression. Levels of seromucoid, C-reactive protein, TNF-α, IL-1β and IL-10 were determined in blood serum. Results: Oral exposure to VNPs was associated with neither elevation of inflammation markers in blood serum nor HSP90α overexpression in the small intestine, i.e. no toxic effects of VNPs were observed. Carrageenan-induced intestinal inflammation was accompanied by higher levels of TNF-α and IL-1β, as well as HSP90α upregulation in the intestinal mucosa, compared with controls. Administration of VNPs to rats with enteritis did not lead to statistically significant changes in concentrations of circulating pro-inflammatory cytokines with the trend towards their increase. Conclusion: No adverse effects were observed in rats orally exposed to VNPs at a dose of 20 μg/kg during two weeks. Using the experimental model of carrageenan-induced enteritis, it was demonstrated that VNPs at the dose used in our study did not affect the course of intestinal inflammation.

Mitigation of IL-1β, IL-6, TNF-α, and markers of apoptosis by ursolic acid against cisplatin-induced oxidative stress and nephrotoxicity in rats

2021 ◽  
Vol 40 (12_suppl) ◽  
pp. S397-S405
Author(s):  
Pankaj Tripathi ◽  
Saeed Alshahrani
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Uric Acid ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Caspase 9 ◽  
Histological Damage ◽  
Tnf Α ◽  
Mda Content ◽  
Pro Inflammatory Cytokines

Background: Ursolic acid (UA) is a natural pentacyclic triterpenoid that is known for its benefits under several pathological conditions. Cisplatin (CP) is among the most preferred chemotherapeutic agents; however, its nephrotoxicity limits its clinical utility. Purpose: This study was aimed to determine the role of UA in the reduction of CP-induced nephrotoxicity and mitigation of pro-inflammatory cytokines and apoptosis in a rat model. Methodology: Male Wistar rats were randomized into vehicle control, CP (7.5 mg/kg), UA 10 mg/kg, and CP with UA 5 and 10 mg/kg groups. Kidney and blood samples were collected for assessment of renal function, measurement of pro-inflammatory cytokines, apoptosis markers, antioxidant activity, and tissue histology. Results: CP significantly increased the levels of serum Cr, BUN, and uric acid; it also induced histological damage reflecting the pathophysiology observed during nephrotoxicity. CP has also shown its pro-oxidant activity in kidney tissue because CP decreased the levels of GSH, SOD, and CAT; it increased the lipid peroxidation as measured by MDA content. In addition, CP significantly upregulated the activity of pro-inflammatory cytokines and expression of apoptotic markers, that is, there were increased levels of IL-1β, IL-6, TNF-α, caspase-3, and caspase-9. Two weeks of continuous treatment of UA showed significant recovery against CP-induced nephrotoxicity; UA decreased the levels of Cr, BUN, and uric acid and ameliorated histological damage. UA also downregulated the activities of IL-1β, IL-6, and TNF-α as well as expression of caspase-3 and caspase-9. Furthermore, CP-induced oxidative stress that was antagonized by UA—the levels of GSH, SOD, and CAT were significantly increased while MDA content was decreased. Conclusions: UA has a protective effect against CP-induced nephrotoxicity, which may be due to its antioxidant activity and mitigation of ILβ-1, ILβ-6, TNF-α, and markers of apoptosis.

141. Can exercise modulate pro-inflammatory cytokines and C-reactive protein in breast cancer survivors? A metaanalysis

2014 ◽  
Vol 40 (11) ◽  
pp. S64
Author(s):  
J. Meneses Echavez ◽  
R. Ramírez Vélez ◽  
E. González Jímenez ◽  
M.J. Sanchéz Pérez ◽  
E. Molina Montes
Keyword(s):  
Breast Cancer ◽  
Cancer Survivors ◽  
Inflammatory Cytokines ◽  
Breast Cancer Survivors ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Pro Inflammatory Cytokines

scholarly journals Ultrasensitive microfluidic array for serum pro-inflammatory cytokines and C-reactive protein to assess oral mucositis risk in cancer patients

2015 ◽  
Vol 407 (23) ◽  
pp. 7239-7243 ◽  
Author(s):  
Colleen E. Krause ◽  
Brunah A. Otieno ◽  
Gregory W. Bishop ◽  
Gayatri Phadke ◽  
Linda Choquette ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Inflammatory Cytokines ◽  
Oral Mucositis ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Pro Inflammatory Cytokines

scholarly journals Pro-inflammatory cytokines and depression in myocardial infarction

2011 ◽  
Vol 10 (2) ◽  
pp. 53-59
Author(s):  
O. L. Barbarash ◽  
N. B. Lebedeva ◽  
V. N. Karetnikova ◽  
S. A. Berns ◽  
V. V. Kashtalap ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Cytokines ◽  
Depression Scale ◽  
Inflammatory Factors ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Reactive Anxiety ◽  
Status Assessment ◽  
Zung Depression Scale ◽  
Pro Inflammatory Cytokines

Aim. To assess the associations between inflammatory factors and anxiety (A) and depression (D) levels in patients with myocardial infarction (MI). Material and methods. The study included 100 MI patients, hospitalised with a diagnosis of Q-wave MI (mean age 62,0±1,3 years). The methods of psychosocial status assessment included Zung depression scale and SpielbergerKhanin personal and reactive anxiety scales. The inflammatory markers of interest included interleukins (IL) 1-beta, IL-6, IL-8, IL-10, and C-reactive protein (CRP). Results. D and A symptoms in the early post-MI stage were associated with higher risk of cardiovascular events in the following year. Among MI patients with comparable MI severity, D and A symptoms were linked to higher levels of pro-inflammatory cytokines IL-1-beta, IL-8, IL-8, and INF-gamma. Conclusion. In MI patients with D and A symptoms, one of the mechanisms of poor prognosis is an activation of subclinical inflammation.

scholarly journals Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

2020 ◽  
Vol 21 (19) ◽  
pp. 7425
Author(s):  
Hyo Young Jung ◽  
Hyun Jung Kwon ◽  
Woosuk Kim ◽  
Kyu Ri Hahn ◽  
Seung Myung Moon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Inflammatory Cytokines ◽  
Neuronal Death ◽  
Microglial Activation ◽  
Ventral Horn ◽  
Phosphoglycerate Mutase ◽  
Ischemic Damage ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Phosphoglycerate mutase 1 (PGAM1) is a glycolytic enzyme that increases glycolytic flux in the brain. In the present study, we examined the effects of PGAM1 in conditions of oxidative stress and ischemic damage in motor neuron-like (NSC34) cells and the rabbit spinal cord. A Tat-PGAM1 fusion protein was prepared to allow easy crossing of the blood-brain barrier, and Control-PGAM1 was synthesized without the Tat peptide protein transduction domain. Intracellular delivery of Tat-PGAM1, not Control-PGAM1, was achieved in a time- and concentration-dependent manner. Immunofluorescent staining confirmed the intracellular expression of Tat-PGAM1 in NSC34 cells. Tat-PGAM1, but not Control-PGAM1, significantly alleviated H2O2-induced oxidative stress, neuronal death, mitogen-activated protein kinase, and apoptosis-inducing factor expression in NSC34 cells. After ischemia induction in the spinal cord, Tat-PGAM1 treatment significantly improved ischemia-induced neurological impairments and ameliorated neuronal cell death in the ventral horn of the spinal cord 72 h after ischemia. Tat-PGAM1 treatment significantly mitigated the ischemia-induced increase in malondialdehyde and 8-iso-prostaglandin F2α production in the spinal cord. In addition, Tat-PGAM1, but not Control-PGAM1, significantly decreased microglial activation and secretion of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α induced by ischemia in the ventral horn of the spinal cord. These results suggest that Tat-PGAM1 can be used as a therapeutic agent to reduce spinal cord ischemia-induced neuronal damage by lowering the oxidative stress, microglial activation, and secretion of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α.

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