scholarly journals Hyperoxalemia Leads to Oxidative Stress in Endothelial Cells and Mice with Chronic Kidney Disease

2021 ◽  
pp. 1-10
Author(s):  
Ke Sun ◽  
Xiaojing Tang ◽  
Shuwei Song ◽  
Yuan Gao ◽  
Hongjing Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Calcification ◽  
Systemic Inflammation ◽  
Inflammatory Factors ◽  
Uremic Toxin ◽  
Inflammatory Factor ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Tnf Α

<b><i>Introduction:</i></b> Cardiovascular disease is the most common cause of morbidity and mortality in patients with ESRD. In addition to phosphate overload, oxalate, a common uremic toxin, is also involved in vascular calcification in patients with ESRD. The present study investigated the role and mechanism of hyperoxalemia in vascular calcification in mice with uremia. <b><i>Methods:</i></b> A uremic atherosclerosis (UA) model was established by left renal excision and right renal electrocoagulation in apoE<sup>−/−</sup> mice to investigate the relationship between oxalate loading and vascular calcification. After 12 weeks, serum and vascular levels of oxalate, vascular calcification, inflammatory factors (TNF-α and IL-6), oxidative stress markers (malondialdehyde [MDA], and advanced oxidation protein products [AOPP]) were assessed in UA mice. The oral oxalate-degrading microbe <i>Oxalobacter formigenes</i> (<i>O. formigenes</i>) was used to evaluate the effect of a reduction in oxalate levels on vascular calcification. The mechanism underlying the effect of oxalate loading on vascular calcification was assessed in cultured human aortic endothelial cells (HAECs) and human aortic smooth muscle cells (HASMCs). <b><i>Results:</i></b> Serum oxalate levels were significantly increased in UA mice. Compared to the control mice, UA mice developed more areas of aortic calcification and showed significant increases in aortic oxalate levels and serum levels of oxidative stress markers and inflammatory factors. The correlation analysis showed that serum oxalate levels were positively correlated with the vascular oxalate levels and serum MDA, AOPP, and TNF-α levels, and negatively correlated with superoxide dismutase activity. The <i>O. formigenes</i> intervention decreased serum and vascular oxalate levels, while did not improve vascular calcification significantly. In addition, systemic inflammation and oxidative stress were also improved in the <i>O. formigenes</i> group. In vitro, high concentrations of oxalate dose-dependently increased oxidative stress and inflammatory factor expression in HAECs, but not in HASMCs. <b><i>Conclusions:</i></b> Our results indicated that hyperoxalemia led to the systemic inflammation and the activation of oxidative stress. The reduction in oxalate levels by <i>O. formigenes</i> might be a promising treatment for the prevention of oxalate deposition in calcified areas of patients with ESRD.

scholarly journals Physiological Responses and Gene Expression in Ultrasound-Guided Supraclavicular Brachial Plexus Block: a Comparative Study

2018 ◽  
Vol 46 (6) ◽  
pp. 2412-2420 ◽  
Author(s):  
Hayam G Sayyed ◽  
Naglaa K. Idriss ◽  
Marwa A. Gaber ◽  
Sherif Sayed ◽  
Rasha Ahmed
Keyword(s):  
Oxidative Stress ◽  
Brachial Plexus Block ◽  
Mrna Levels ◽  
Oxidative Stress Markers ◽  
Ultrasound Guided ◽  
Stress Markers ◽  
Pain Scores ◽  
Tnf Α ◽  
Supraclavicular Brachial Plexus Block ◽  
Plexus Block

Background/Aims: Ultrasound-guided supraclavicular brachial plexus block (BPB) has come into wider use as a regional anesthetic during upper limb operations. This study assessed the neurological and hemodynamic changes and gene expression after co-administration of midazolam or neostigmine with bupivacaine during supraclavicular BPB. Methods: The study involved 90 adults divided into three groups: control (bupivacaine), midazolam (bupivacaine plus midazolam), and neostigmine (bupivacaine plus neostigmine). Blood samples were taken and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) mRNA levels were measured by real-time PCR, and oxidative stress markers were identified. In addition to the hemodynamic variables, the onset and duration of sensory and motor blockades, duration of analgesia, pain scores, time of first request for an analgesic, and amounts of analgesics ingested were evaluated. Results: Compared with the control and neostigmine groups, the midazolam group experienced longer sensory and motor blockades, prolonged analgesia, lower pain scores at 12 h and 24 h, and lower need for postoperative analgesics. Moreover, the midazolam group exhibited lower oxidative stress markers with a higher fold change in IL-6 and TNF-α mRNA levels. Conclusion: Midazolam co-administered with bupivacaine provided better analgesic quality than did neostigmine with bupivacaine. This might be due to its superior antioxidant and anti-inflammatory effects.

Phosphate overload directly induces systemic inflammation and malnutrition as well as vascular calcification in uremia

2014 ◽  
Vol 306 (12) ◽  
pp. F1418-F1428 ◽  
Author(s):  
Shunsuke Yamada ◽  
Masanori Tokumoto ◽  
Narihito Tatsumoto ◽  
Masatomo Taniguchi ◽  
Hideko Noguchi ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Systemic Inflammation ◽  
Premature Death ◽  
Cardiovascular Death ◽  
Tissue Levels ◽  
Stress Markers ◽  
Increased Risk ◽  
Tnf Α ◽  
Promising Treatment ◽  
Almost All

Hyperphosphatemia contributes to increased cardiovascular mortality through vascular calcification (VC) in patients with chronic kidney disease (CKD). Malnutrition and inflammation are also closely linked to an increased risk of cardiovascular death in CKD. However, the effects of Pi overload on inflammation and malnutrition remain to be elucidated. The aim of the present study was to investigate the effects of dietary Pi loading on the interactions among inflammation, malnutrition, and VC in CKD. We used control rats fed normal diets and adenine-induced CKD rats fed diets with different Pi concentrations ranging from 0.3% to 1.2% for 8 wk. CKD rats showed dietary Pi concentration-dependent increases in serum and tissue levels of TNF-α and urinary and tissue levels of oxidative stress markers and developed malnutrition (decrease in body weight, serum albumin, and urinary creatinine excretion), VC, and premature death without affecting kidney function. Treatment with 6% lanthanum carbonate blunted almost all changes induced by Pi overload. Regression analysis showed that serum Pi levels closely correlated with the extent of inflammation, malnutrition, and VC. Also, in cultured human vascular smooth muscle cells, high-Pi medium directly increased the expression of TNF-α in advance of the increase in osteochondrogenic markers. Our data suggest that dietary Pi overload induces systemic inflammation and malnutrition, accompanied by VC and premature death in CKD, and that inhibition of Pi loading through dietary or pharmacological interventions or anti-inflammatory therapy may be a promising treatment for the prevention of malnutrition-inflammation-atherosclerosis syndrome.

scholarly journals Inflammation and its association with oxidative stress in dogs with heart failure

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Alenka Nemec Svete ◽  
Barbara Verk ◽  
Nina Čebulj-Kadunc ◽  
Janez Salobir ◽  
Vida Rezar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Blood Cell ◽  
White Blood Cell ◽  
Interleukin 6 ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
And Oxidative Stress

Abstract Background Inflammation and oxidative stress can contribute to the development and progression of heart failure. This study aimed to investigate the association between inflammatory and oxidative stress markers in dogs with congestive heart failure (CHF). Associations between the disease severity marker N-terminal pro-B-type natriuretic peptide (NT-proBNP) and markers of inflammation and oxidative stress were also determined. Results Thirty-seven dogs with cardiovascular diseases (dilated cardiomyopathy, DCM (16 dogs), myxomatous mitral valve disease, MMVD (21 dogs)) and ten healthy dogs were included in this prospective study. The patients were further divided into groups with (26) and without CHF (11). We found a significantly higher serum concentration of C-reactive protein (P = 0.012), white blood cell (P = 0.001), neutrophil (P = 0.001) and monocyte counts (P = 0.001) in patients with CHF compared to control dogs. The concentration of tumor necrosis factor-alpha (TNF-α) was significantly higher in patients with CHF compared to patients without CHF (P = 0.030). No significant difference was found in most of the measured parameters between MMVD and DCM patients, except for glutathione peroxidase (GPX) and NT-proBNP. In patients with CHF, TNF-α correlated positively with malondialdehyde (P = 0.014, r = 0.474) and negatively with GPX (P = 0.026, r = − 0.453), and interleukin-6 correlated negatively with GPX (P = 0.046, r = − 0.412). NT-proBNP correlated positively with malondialdehyde (P = 0.011, r = 0.493). In patients without CHF none of the inflammatory and oxidative stress markers correlated significantly. Furthermore, in the group of all cardiac patients, GPX activity significantly negatively correlated with NT-proBNP (P = 0.050, r = − 0.339) and several markers of inflammation, including TNF-α (P = 0.010, r = − 0.436), interleukin-6 (P = 0.026, r = − 0.382), white blood cell (P = 0.032, r = − 0.369), neutrophil (P = 0.027, r = − 0.379) and monocyte counts (P = 0.024, r = − 0.386). Conclusion Inflammatory and oxidative stress markers are linked in canine CHF patients, but not in patients without CHF. These results suggest complex cross communication between the two biological pathways in advanced stages of CHF.

scholarly journals Correlations of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases in gingival crevicular fluid with peri-implantitis

2019 ◽  
Vol 17 ◽  
pp. 205873921984554
Author(s):  
Zhiming Song ◽  
Paul Weigl ◽  
Bi Wang
Keyword(s):  
Oxidative Stress ◽  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Gingival Crevicular Fluid ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Probing Depth ◽  
Tnf Α ◽  
Hs Crp ◽  
Crevicular Fluid

This study aimed to analyze the correlations of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases (MMPs) in gingival crevicular fluid (GCF) with peri-implantitis (PI). Forty patients receiving dental implantation were enrolled. There were 52 implants, which were divided into PI group (42 implants) and health implant (HI) group (10 implants). Fifty-two healthy teeth (HT) with the same names with affected teeth in the patients were selected as the control group. The periodontal status was recorded. The GCF was collected and quantified. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), hypersensitive C-reactive protein (hs-CRP), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), MMP-13, and MMP-8 were detected using enzyme-linked immunosorbent assay (ELISA). Results showed that the probing depth, sulcus bleeding index, GCF volume, and TNF-α, IL-6, hs-CRP, MMP-8, and MMP-13 levels in GCF in PI group were significantly higher than HI and HT groups, respectively ( P < 0.01 or P < 0.05). The SOD and GSH-Px levels in PI group were significantly lower than HI and HT groups, respectively ( P < 0.05). Excepting hs-CRP, there was no significant difference of each index between HI and HT groups ( P > 0.05). In conclusion, TNF-α, IL-6, hs-CRP, SOD, GSH-Px, MMP-8, and MMP-13 are involved in the occurrence of PI, and they may be used as auxiliary indicators to evaluate the degree of PI. In addition, the clinical periodontal index probing depth and sulcus bleeding index are positively correlated with GCF volume, hs-CRP, MMP-8, and MMP-13.

scholarly journals Inflammation and its association with oxidative stress in dogs with heart failure

2020 ◽  
Author(s):  
Alenka Nemec Svete ◽  
Barbara Verk ◽  
Nina Čebulj-Kadunc ◽  
Janez Salobir ◽  
Vida Rezar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Blood Cell ◽  
White Blood Cell ◽  
Interleukin 6 ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
And Oxidative Stress

Abstract Background Inflammation and oxidative stress can contribute to the development and progression of heart failure. This study aimed to investigate the association between inflammatory and oxidative stress markers in dogs with congestive heart failure (CHF). Associations between the disease severity marker N-terminal pro-B-type natriuretic peptide (NT-proBNP) and markers of inflammation and oxidative stress were also determined. Results Thirty-seven dogs with cardiovascular diseases (dilated cardiomyopathy (16 dogs), myxomatous mitral valve disease (21 dogs)) and ten healthy dogs were included in this prospective study. The patients were further divided into groups with (26) and without CHF (11). We found a significantly higher serum concentration of C-reactive protein (P = 0.012), white blood cell (P = 0.001), neutrophil (P = 0.001) and monocyte counts (P = 0.001) in patients with CHF compared to control dogs. The concentration of tumor necrosis factor-alpha (TNF-α) was significantly higher in patients with CHF compared to patients without CHF (P = 0.030). In patients with CHF, TNF-α correlated positively with malondialdehyde (P = 0.014, r = 0.474) and negatively with glutathione peroxidase (GPX) (P = 0.026, r = − 0.453), and interleukin-6 correlated negatively with GPX (P = 0.046, r = − 0.412). NT -proBNP correlated positively with malondialdehyde (P = 0.011, r = 0.493). In patients without CHF none of the inflammatory and oxidative stress markers correlated significantly. Furthermore, in the group of all cardiac patients, GPX activity significantly negatively correlated with NT-proBNP (P = 0.050, r = − 0.339) and several markers of inflammation, including TNF–α (P = 0.010, r = − 0.436), interleukin-6 (P = 0.026, r = − 0.382), white blood cell (P = 0.032, r = − 0.369), neutrophil (P = 0.027, r = − 0.379) and monocyte counts (P = 0.024, r = − 0.386). Conclusion Inflammatory and oxidative stress markers are linked in canine CHF patients, but not in patients without CHF. These results suggest complex cross communication between the two biological pathways in advanced stages of CHF.

scholarly journals Neurotrophins, cytokines, oxidative stress mediators and mood state in bipolar disorder: systematic review and meta-analyses

2018 ◽  
Vol 213 (3) ◽  
pp. 514-525 ◽  
Author(s):  
Tobias Rowland ◽  
Benjamin I. Perry ◽  
Rachel Upthegrove ◽  
Nicholas Barnes ◽  
Jayanta Chatterjee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Bipolar Disorder ◽  
Inflammatory Markers ◽  
Healthy Controls ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Tnf Α ◽  
Meta Analyses ◽  
And Oxidative Stress

BackgroundA reliable biomarker signature for bipolar disorder sensitive to illness phase would be of considerable clinical benefit. Among circulating blood-derived markers there has been a significant amount of research into inflammatory markers, neurotrophins and oxidative stress markers.AimsTo synthesise and interpret existing evidence of inflammatory markers, neurotrophins and oxidative stress markers in bipolar disorder focusing on the mood phase of illness.MethodFollowing PRISMA (Preferred Reporting Items for Systematic reviews and Meta-analyses) guidelines, a systematic review was conducted for studies investigating peripheral biomarkers in bipolar disorder compared with healthy controls. We searched Medline, Embase, PsycINFO, SciELO and Web of Science, and separated studies by bipolar mood phase (mania, depression and euthymia). Extracted data on each biomarker in separate mood phases were synthesised using random-effects model meta-analyses.ResultsIn total, 53 studies were included, comprising 2467 cases and 2360 controls. Fourteen biomarkers were identified from meta-analyses of three or more studies. No biomarker differentiated mood phase in bipolar disorder individually. Biomarker meta-analyses suggest a combination of high-sensitivity C-reactive protein/interleukin-6, brain derived neurotrophic factor/tumour necrosis factor (TNF)-α and soluble TNF-α receptor 1 can differentiate specific mood phase in bipolar disorder. Several other biomarkers of interest were identified.ConclusionsCombining biomarker results could differentiate individuals with bipolar disorder from healthy controls and indicate a specific mood-phase signature. Future research should seek to test these combinations of biomarkers in longitudinal studies.Declaration of interestNone.

β-Amyrin, a pentacyclic triterpene, exhibits anti-fibrotic, anti-inflammatory, and anti-apoptotic effects on dimethyl nitrosamine–induced hepatic fibrosis in male rats

2016 ◽  
Vol 36 (2) ◽  
pp. 113-122 ◽  
Author(s):  
A Thirupathi ◽  
PC Silveira ◽  
RT Nesi ◽  
RA Pinho
Keyword(s):  
Oxidative Stress ◽  
Hepatic Fibrosis ◽  
Caspase 3 ◽  
Inflammatory Marker ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Male Rats ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Tnf Α ◽  
Anti Inflammatory

Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Attenuation of fibrogenic process can significantly lower the mortality rate. However, pharmaceutical intervention at fibrogenesis stage remains a major task in medicine. So there is a need for a natural compound to treat hepatic fibrosis. This study was outlined to investigate the anti-fibrotic effect of β-amyrin in dimethylnitrosamine (DMN)-induced hepatic fibrosis male rats. Serum liver function markers (aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase), oxidative stress markers (malondialdehyde, superoxide dismutase, catalase, glutathione peroxidase, glutathione reduced content and vitamin C), tissue inflammatory marker (tumor necrosis factor α (TNF-α)), apoptosis marker (caspase 3) and fibrolytic marker (tissue inhibitor of metalloproteinase 1 (TIMP-1)) were evaluated before and after β-amyrin treatment in DMN-induced rat. β-Amyrin treatment attenuated the altered levels of the serum enzyme markers produced by DMN and caused a subsequent recovery toward normalization. Oxidative stress markers and TNF-α levels were reduced significantly ( p < 0.001) as well as proteins’ (caspase-3 and TIMP-1) expression was reduced in β-amyrin –treated DMN rats. By virtue of β-amyrin properties of inhibiting oxidative stress, apoptosis, inflammation, and fibrogenesis, it might act as an ideal anti-inflammatory and anti-fibrogenic agent to halt the progression of liver fibrosis to chronicity.

scholarly journals Topamax® and Ginger Oil Potential Neurotoxicity And Their Interaction in Mice Thru Oxidative Stress and Inflammatory Markers, Neurotransmitters Expression and Immunohistochemical Measurements

2022 ◽  
Author(s):  
Dalia M Mabrouk ◽  
Aida El makawy ◽  
Kawkab A Ahmed ◽  
Faten M Ibrahim
Keyword(s):  
Oxidative Stress ◽  
Histopathological Examination ◽  
Immune Reactivity ◽  
Mrna Levels ◽  
Oxidative Stress Markers ◽  
Gamma Aminobutyric Acid ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α ◽  
Factor Alpha

Abstract Background: Topamax® ® has multiple pharmacological mechanisms that are efficient to treat epilepsy and migraine. Ginger has been demonstrated to have gingerols and shogaols compounds that proven to cross the blood-brain barrier causing migraine relief, implying that it is useful in the treatment of migraines. Moreover, Topamax has many off-label uses. So it was necessary to explore the possible neurotoxicity of Topamax®, Ginger oil and their interaction in the mice brain. Methods and Results: Male mice were orally gavage with Topamax®, ginger oil (400mg/kg), and Topamax® plus ginger oil with the same pattern for one month. Oxidative stress markers, acetylcholinesterase (AchE) and gamma aminobutyric acid (GABA) and tumor necrosis factor-alpha (TNF- α), were analyzed in brain tissue. Histopathological examination by hematoxylin and eosin, immunohistochemical glial fibrillary acidic protein (GFAP), and Bax expression analysis were done. The mRNA levels of GABAAR subunits, Gabra1, Gabra3, and Gabra5 were evaluated by RT qPCR. The analysis of data revealed that Topamax® elevated the levels of oxidative stress markers, neurotransmitters, TNF-α, and diminished the level of glutathione reduced (GSH). Topamax® exhibited various neuropathological alterations, strong Bax expression, and GFAP immune-reactivity in the cerebral cortex. The interaction effect of Topamax® plus ginger oil attenuated the changes induced by Topamax® in the abovementioned parameters. Both Topamax® and ginger oil upregulated the mRNA expression of gabra1 and gabra3 while their interaction markedly downregulated them. Conclusion: We can conclude that the Topamax® overdose could possibly cause neurotoxicity, but the interaction with ginger oil can reduce Topamax® -induced neurotoxicity and should be taken in parallel.

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