scholarly journals Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1303
Author(s):  
Vittorio Calabrese ◽  
Maria Scuto ◽  
Angela Trovato Salinaro ◽  
Giuseppe Dionisio ◽  
Sergio Modafferi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Brain Injuries ◽  
Redox Homeostasis ◽  
Critical Role ◽  
Sirtuin 1 ◽  
Inflammatory Processes ◽  
History Of ◽  
Metabolic Interactions ◽  
Factor Α

Emerging evidence indicates that the dysregulation of cellular redox homeostasis and chronic inflammatory processes are implicated in the pathogenesis of kidney and brain disorders. In this light, endogenous dipeptide carnosine (β-alanyl-L-histidine) and hydrogen sulfide (H2S) exert cytoprotective actions through the modulation of redox-dependent resilience pathways during oxidative stress and inflammation. Several recent studies have elucidated a functional crosstalk occurring between kidney and the brain. The pathophysiological link of this crosstalk is represented by oxidative stress and inflammatory processes which contribute to the high prevalence of neuropsychiatric disorders, cognitive impairment, and dementia during the natural history of chronic kidney disease. Herein, we provide an overview of the main pathophysiological mechanisms related to high levels of pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and neurotoxins, which play a critical role in the kidney–brain crosstalk. The present paper also explores the respective role of H2S and carnosine in the modulation of oxidative stress and inflammation in the kidney–brain axis. It suggests that these activities are likely mediated, at least in part, via hormetic processes, involving Nrf2 (Nuclear factor-like 2), Hsp 70 (heat shock protein 70), SIRT-1 (Sirtuin-1), Trx (Thioredoxin), and the glutathione system. Metabolic interactions at the kidney and brain axis level operate in controlling and reducing oxidant-induced inflammatory damage and therefore, can be a promising potential therapeutic target to reduce the severity of renal and brain injuries in humans.

scholarly journals Lactobacillus plantarum Exhibits Antioxidant and Cytoprotective Activities in Porcine Intestinal Epithelial Cells Exposed to Hydrogen Peroxide

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jing Wang ◽  
Wei Zhang ◽  
Sixin Wang ◽  
Yamin Wang ◽  
Xu Chu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Lactobacillus Plantarum ◽  
Redox Homeostasis ◽  
Critical Role ◽  
Probiotic Bacterium ◽  
Related Factor ◽  
H2o2 Treatment

Probiotics are widely used for protection against stress-induced intestinal dysfunction. Oxidative stress plays a critical role in gastrointestinal disorders. It is established that probiotics alleviate oxidative stress; however, the mechanism of action has not been elucidated. We developed an in vitro intestinal porcine epithelial cells (IPEC-J2) model of oxidative stress to explore the antioxidant effect and potential mode of action of Lactobacillus plantarum ZLP001. The IPEC-J2 cells were preincubated with and without L. plantarum ZLP001 for 3 h and then exposed to hydrogen peroxide (H2O2) for 4 h. Pretreatment with L. plantarum ZLP001 protected IPEC-J2 cells against H2O2-induced oxidative damage as indicated by cell viability assays and significantly alleviated apoptosis elicited by H2O2. L. plantarum ZLP001 pretreatment decreased reactive oxygen species production and the cellular malondialdehyde concentration and increased the mitochondrial membrane potential compared with H2O2 treatment alone, suggesting that L. plantarum ZLP001 promotes the maintenance of redox homeostasis in the cells. Furthermore, L. plantarum ZLP001 regulated the expression and generation of some antioxidant enzymes, thereby activating the antioxidant defense system. Treatment with L. plantarum ZLP001 led to nuclear erythroid 2-related factor 2 (Nrf2) enrichment in the nucleus compared with H2O2 treatment alone. Knockdown of Nrf2 significantly weakened the alleviating effect of L. plantarum ZLP001 on antioxidant stress in IPEC-J2 cells, suggesting that Nrf2 is involved in the antioxidative effect of L. plantarum ZLP001. Collectively, these results indicate that L. plantarum ZLP001 is a promising probiotic bacterium that can potentially alleviate oxidative stress.

scholarly journals Oxidative Stress and Thrombosis during Aging: The Roles of Oxidative Stress in RBCs in Venous Thrombosis

2020 ◽  
Vol 21 (12) ◽  
pp. 4259
Author(s):  
Qinhong Wang ◽  
Rahima Zennadi
Keyword(s):  
Oxidative Stress ◽  
Venous Thrombosis ◽  
Life Stage ◽  
Redox Homeostasis ◽  
Critical Role ◽  
Membrane Integrity ◽  
Accelerated Aging ◽  
Coagulation Factors ◽  
Membrane Structure And Function

Mid-life stage adults are at higher risk of developing venous thrombosis (VT)/thromboembolism (VT/E). Aging is characterized by an overproduction of reactive oxygen species (ROS), which could evoke a series of physiological changes involved in thrombosis. Here, we focus on the critical role of ROS within the red blood cell (RBC) in initiating venous thrombosis during aging. Growing evidence has shifted our interest in the role of unjustifiably unvalued RBCs in blood coagulation. RBCs can be a major source of oxidative stress during aging, since RBC redox homeostasis is generally compromised due to the discrepancy between prooxidants and antioxidants. As a result, ROS accumulate within the RBC due to the constant endogenous hemoglobin (Hb) autoxidation and NADPH oxidase activation, and the uptake of extracellular ROS released by other cells in the circulation. The elevated RBC ROS level affects the RBC membrane structure and function, causing loss of membrane integrity, and decreased deformability. These changes impair RBC function in hemostasis and thrombosis, favoring a hypercoagulable state through enhanced RBC aggregation, RBC binding to endothelial cells affecting nitric oxide availability, RBC-induced platelet activation consequently modulating their activity, RBC interaction with and activation of coagulation factors, increased RBC phosphatidylserine exposure and release of microvesicles, accelerated aging and hemolysis. Thus, RBC oxidative stress during aging typifies an ultimate mechanism in system failure, which can affect major processes involved in the development of venous thrombosis in a variety of ways. The reevaluated concept of the critical role of RBC ROS in the activation of thrombotic events during aging will help identify potential targets for novel strategies to prevent/reduce the risk for VT/E or VT/E recurrences in mid-life stage adults.

Red wine extract protects against oxidative-stress-induced endothelial senescence

2012 ◽  
Vol 123 (8) ◽  
pp. 499-507 ◽  
Author(s):  
Ilse P. G. Botden ◽  
Hisko Oeseburg ◽  
Matej Durik ◽  
Frank P. J. Leijten ◽  
Leonie C. Van Vark-Van Der Zee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Red Wine ◽  
Umbilical Vein ◽  
Critical Role ◽  
Sirtuin 1 ◽  
Mrna Levels ◽  
Nitric Oxide Synthase Inhibitor ◽  
Age Related ◽  
Cox 2

Red wine polyphenols may preserve endothelial function during aging. Endothelial cell senescence enhances age-related endothelial dysfunction. We investigated whether RWE (red wine extract) prevents oxidative-stress-induced senescence in HUVECs (human umbilical-vein endothelial cells). Senescence was induced by exposing HUVECs to tBHP (t-butylhydroperoxide), and quantified by senescence-associated β-galactosidase staining. RWE (0–50 μg/ml) concentration dependently decreased senescence by maximally 33±7.1%. RWE prevented the senescence-associated increase in p21 protein expression, inhibited tBHP-induced DNA damage of endothelial cells and induced relaxation of PCAs (porcine coronary arteries). Inhibition of SIRT1 (sirtuin 1) by sirtinol partially reversed the effect of RWE on tBHP-induced senescence, whereas both the NOS (nitric oxide synthase) inhibitor L-NMMA (NG-monomethyl-L-arginine) and the COX (cyclo-oxygenase) inhibitor indomethacin fully inhibited it. Furthermore, incubation of HUVECs with RWE increased eNOS (endothelial NOS) and COX-2 mRNA levels as well as phosphorylation of eNOS at Ser1177. RWE protects endothelial cells from tBHP-induced senescence. NO and COX-2, in addition to activation of SIRT1, play a critical role in the inhibition of senescence induction in human endothelial cells by RWE.

scholarly journals PEA/Polydatin: Anti-Inflammatory and Antioxidant Approach to Counteract DNBS-Induced Colitis

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 464
Author(s):  
Alessio Filippo Peritore ◽  
Ramona D’Amico ◽  
Marika Cordaro ◽  
Rosalba Siracusa ◽  
Roberta Fusco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Clinical Signs ◽  
Neutrophil Infiltration ◽  
Sirtuin 1 ◽  
Positive Staining ◽  
Related Factor ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Inflammatory Processes ◽  
Anti Inflammatory

Palmitoylethanolamide (PEA) has well-known anti-inflammatory effects. However, PEA does not possess an antioxidant ability. A comicronized formulation of ultramicronized PEA (um-PEA) and polydatin (Pol) PEA/Pol, a biological precursor of resveratrol with antioxidant activity, could have protective effects on oxidative stress produced by inflammatory processes. We evaluated the effects of a comicronized PEA/Pol 10 mg/kg (9 mg of um-PEA+1 mg of polydatin) in a model of Dinitrobenzene sulfonic acid (DNBS)-induced colitis. Ulcerative colitis was induced in mice by intrarectally injection of DNBS (4 mg in 100 µL of 50% ethanol per mouse). Macroscopic and histologic colon alterations and marked clinical signs were observed four days after DNBS and elevated cytokine production. The myeloperoxidase (MPO) activity assessed for neutrophil infiltration was associated with ICAM-1 and P-selectin adhesion controls in colons. Oxidative stress was detected with increased poly ADP-ribose polymerase (PARP) and nitrotyrosine positive staining and malondialdehyde (MDA) levels in inflamed colons. Macroscopic and histologic alterations minimized by oral PEA/Pol, as well as neutrophil infiltration, inflammatory cytokine release, MDA, nitrotyrosine, PARP and ICAM-1, and P-selectin expressions. The mechanism of action of PEA/Pol could be related to the sirtuin 1/nuclear factor erythroid 2-related factor 2 (SIRT-1/Nrf2) pathway and nuclear factor (NF)-κB. PEA/Pol administration inhibited NF-κB and increased SIRT-1/Nrf2 expressions. Our results show that PEA/Pol is capable of decreasing inflammatory bowel disease (IBD) DNBS-induced in mice.

The Role of Inflammation in Neurological Disorders

2018 ◽  
Vol 24 (14) ◽  
pp. 1485-1501 ◽  
Author(s):  
Diana Degan ◽  
Raffaele Ornello ◽  
Cindy Tiseo ◽  
Antonio Carolei ◽  
Simona Sacco ◽  
...  
Keyword(s):  
Brain Injuries ◽  
Wide Spectrum ◽  
Neurological Diseases ◽  
Myelin Proteins ◽  
Immune Mediated ◽  
Inflammatory Processes ◽  
History Of ◽  
Neurological Conditions ◽  
Lateral Sclerosis

Traditionally neurological diseases have been classified, on the basis of their pathogenesis, into vascular, degenerative, inflammatory and traumatic diseases. Examples of the main inflammatory neurological diseases include multiple sclerosis, which is characterized by an immune-mediated response against myelin proteins, and meningoencephalitis, where the inflammatory response is triggered by infectious agents. However, recent evidence suggests a potential role of inflammatory mechanisms also in neurological conditions not usually categorized as inflammatory, such as Alzheimer’s disease, Parkinson’s disease, Huntington’ disease, amyotrophic lateral sclerosis, stroke and traumatic brain injuries. The activation of glial cells and of complement-mediated pathways, the synthesis of inflammation mediators, and the recruitment of leukocytes are the key elements of secondary inflammatory injury following a wide spectrum of primary brain injuries. A better understanding of the role that inflammatory processes play in the natural history of diseases is essential in order to identify potential therapeutic targets and to develop integrated pharmacological approaches acting at different levels and stages of the diseases.

scholarly journals Functional dichotomy of A20 in apoptotic and necrotic cell death

2005 ◽  
Vol 387 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Peter STORZ ◽  
Heike DÖPPLER ◽  
Christiane FERRAN ◽  
Shane T. GREY ◽  
Alex TOKER
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Stress Responses ◽  
Zinc Finger Protein ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Inhibitory Protein ◽  
Cellular Survival ◽  
Factor Α ◽  
Oxidative Stress Responses

ROS (reactive oxygen species) play important roles in the progression of a number of human pathologies. ROS promote cell death, but can also induce gene transcription. The transcription factor NF-κB (nuclear factor κB) plays a critical role in oxidative stress responses. One of the proteins regulated by NF-κB is the zinc-finger protein A20. In TNF (tumour necrosis factor)-α signalling, NF-κB induction of A20 leads to increased cell survival. In the present paper, we show that in response to oxidative stress, A20 actually enhances cell death by necrosis, but not by apoptosis. Exposure of cells to ROS leads to the up-regulation of A20 which acts via a negative-feedback loop to block NF-κB activation and cellular survival. Silencing of A20 by RNAi (RNA interference) increases both the induction of NF-κB and the subsequent survival of cells exposed to high doses of oxidative stress, which, in untreated cells, promotes death by necrosis. Cells which express high basal levels of A20 are less protected from oxidative-stress-induced cell death when compared with cells with lower A20 expression. We also show that A20 regulates NF-κB by blocking the degradation of IκB (inhibitory protein κB) α. These data highlight a novel role for A20 in oxidative stress responses by terminating NF-κB-dependent survival signalling and thus sensitizing cells to death by necrosis.

Oxidative stress in Fanconi anaemia: from cells and molecules towards prospects in clinical management

2012 ◽  
Vol 393 (1-2) ◽  
pp. 11-21 ◽  
Author(s):  
Giovanni Pagano ◽  
Annarita Aiello Talamanca ◽  
Giuseppe Castello ◽  
Federico V. Pallardó ◽  
Adriana Zatterale ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Dna Damage ◽  
Bone Marrow Failure ◽  
Redox Homeostasis ◽  
White Blood Cells ◽  
Oxygen Toxicity ◽  
Fanconi Anaemia ◽  
Excess Oxygen ◽  
Clinical Complications ◽  
Factor Α

Abstract Fanconi anaemia (FA) is a genetic disease featuring bone marrow failure, proneness to malignancies, and chromosomal instability. A line of studies has related FA to oxidative stress (OS). This review attempts to evaluate the evidence for FA-associated redox abnormalities in the literature from 1981 to 2010. Among 2170 journal articles on FA evaluated, 162 related FA with OS. Early studies reported excess oxygen toxicity in FA cells that accumulated oxidative DNA damage. Prooxidant states were found in white blood cells and body fluids from FA patients as excess luminol-dependent chemiluminescence, 8-hydroxy-deoxyguanosine, reduced glutathione/oxidized glutathione imbalance, and tumour necrosis factor-α. Some FA gene products involved in redox homeostasis can be summarized as follows: (a) FANCA, FANCC, and FANCG interact with cytochrome P450-related activities and/or respond to oxidative damage; (b) FANCD2 in OS response interacts with forkhead box O3 and ataxia telangiectasia mutated protein; (c) FANCG is found in mitochondria and interacts with PRDX3, and FA-G cells display distorted mitochondria and decreased peroxidase activity; (d) FANCJ (BACH1/BRIP1) is a repressor of haeme oxygenase-1 gene and senses oxidative base damage; (e) antioxidants, such as tempol and resveratrol decrease cancer incidence and haematopoietic defects in Fancd2-/- mice. The overall evidence for FA-associated OS may suggest designing chemoprevention studies aimed at delaying the onset of OS-related clinical complications.

scholarly journals Validation of a Concussion Assessment Tool

Neurology ◽  
2019 ◽  
Vol 93 (14 Supplement 1) ◽  
pp. S2.1-S2
Author(s):  
Sasidharan Taravath ◽  
Megan Peedin ◽  
Mark Williams ◽  
Len Lecci ◽  
Julian Keith
Keyword(s):  
Performance Test ◽  
Brain Injuries ◽  
Assessment Tool ◽  
Critical Role ◽  
Continuous Performance Test ◽  
Assessment Tools ◽  
Screening And Identification ◽  
History Of ◽  
Neurocognitive Test ◽  
Pediatric Neurologist

ObjectiveSports related concussions, or mild traumatic brain injuries, have been steadily increasing over the past two decades. Effective screening and identification of concussions play a critical role in the diagnosis and rehabilitation process. Although side line assessment tools are available, there are few well validated tests available to assist medical providers in this decision-making process. This study aims to determine whether previously validated tools which assess neurocognitive and neurophysiological abilities can predict concussion symptom endorsement in a sample of child and adolescent athletes.BackgroundParticipants were recruited from two settings: The office of a pediatric neurologist (seen 3 to 109 days post incident) and from preseason baseline assessments.Design/MethodsMethod: Participants were 113 individuals, aged 6 to 17, representing 84 consecutive cases of individuals completing standardized baseline assessments with no recent history of concussion, and 29 consecutive cases undergoing a post-concussion evaluation by a pediatric neurologist. Participants completed a standardized battery of tests comprised of the Connors’ Continuous Performance Test (CPT-3), the Balance Error Scoring System (BESS) and the NIH 4-meter Gait Test and completed a checklist of CDC concussion symptoms.ResultsThe screening battery explained 33% of the variance (d = 1.4) in concussion symptom endorsement, after controlling for age. The neurocognitive test alone (CPT-3) accounts for 21.5% of the variance (d = 1.05) in symptoms after controlling for age, and the neurobehavioral measures (BESS and NIH 4m Gait) then account for an additional 11.5% variance (they account for 18.6% variance, d = 0.96, when entered first). These effect sizes are considered large to very large and reflect a marked increase in predictive validity relative to existing measures used in concussion assessments.ConclusionsAn easy to administer and relatively brief screening test can be used in medical settings to identify concussions and predict significant and substantial variability in CDC concussion symptoms.

scholarly journals Exercise and the Aging Endothelium

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Saeid Golbidi ◽  
Ismail Laher
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Health ◽  
Critical Role ◽  
Mortality Rates ◽  
Favorable Effect ◽  
Ageing Population ◽  
Functional Aspect ◽  
Gradual Decline ◽  
Age Related ◽  
Inflammatory Processes

The endothelium plays a critical role in the maintenance of cardiovascular health by producing nitric oxide and other vasoactive materials. Aging is associated with a gradual decline in this functional aspect of endothelial regulation of cardiovascular homeostasis. Indeed, age is an independent risk factor for cardiovascular diseases and is in part an important factor in the increased exponential mortality rates from vascular disease such as myocardial infarction and stroke that occurs in the ageing population. There are a number of mechanisms suggested to explain age-related endothelial dysfunction. However, recent scientific studies have advanced the notion of oxidative stress and inflammation as the two major risk factors underlying aging and age-related diseases. Regular physical activity, known to have a favorable effect on cardiovascular health, can also improve the function of the ageing endothelium by modulating oxidative stress and inflammatory processes, as we discuss in this paper.

scholarly journals Prediabetic Nephropathy as an Early Consequence of the High-Calorie/High-Fat Diet: Relation to Oxidative Stress

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1152-1161 ◽  
Author(s):  
Hanna Shevalye ◽  
Sergey Lupachyk ◽  
Pierre Watcho ◽  
Roman Stavniichuk ◽  
Khaled Khazim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Renal Cortex ◽  
Fold Increase ◽  
Sirtuin 1 ◽  
Initiation Factor ◽  
High Fat ◽  
Alimentary Obesity ◽  
Factor Α ◽  
High Calorie

This study evaluated early renal functional, structural, and biochemical changes in high-calorie/high-fat diet fed mice, a model of prediabetes and alimentary obesity. Male C57BL6/J mice were fed normal (11 kcal% fat) or high-fat (58 kcal% fat) diets for 16 wk. Renal changes were evaluated by histochemistry and immunohistochemistry, Western blot analysis, ELISA, enzymatic assays, and chemiluminometry. High-fat diet consumption led to increased body and kidney weights, impaired glucose tolerance, hyperinsulinemia, polyuria, a 2.7-fold increase in 24-h urinary albumin excretion, 20% increase in renal glomerular volume, 18% increase in renal collagen deposition, and 8% drop of glomerular podocytes. It also resulted in a 5.3-fold increase in urinary 8-isoprostane excretion and a 38% increase in renal cortex 4-hydroxynonenal adduct accumulation. 4-hydroxynonenal adduct level and immunoreactivity or Sirtuin 1 expression in renal medulla were not affected. Studies of potential mechanisms of the high-fat diet induced renal cortex oxidative injury revealed that whereas nicotinamide adenine dinucleotide phosphate reduced form oxidase activity only tended to increase, 12/15-lipoxygenase was significantly up-regulated, with approximately 12% increase in the enzyme protein expression and approximately 2-fold accumulation of 12(S)-hydroxyeicosatetraenoic acid, a marker of 12/15-lipoxygenase activity. Accumulation of periodic acid-Schiff -positive material, concentrations of TGF-β, sorbitol pathway intermediates, and expression of nephrin, CAAT/enhancer-binding protein homologous protein, phosphoeukaryotic initiation factor-α, and total eukaryotic initiation factor-α in the renal cortex were indistinguishable between experimental groups. Vascular endothelial growth factor concentrations were reduced in high-fat diet fed mice. In conclusion, systemic and renal cortex oxidative stress associated with 12/15-lipoxygenase overexpression and activation is an early phenomenon caused by high-calorie/high-fat diet consumption and a likely contributor to kidney disease associated with prediabetes and alimentary obesity.

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