scholarly journals “Cumulative Stress”: The Effects of Maternal and Neonatal Oxidative Stress and Oxidative Stress-Inducible Genes on Programming of Atopy

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Sara Manti ◽  
Lucia Marseglia ◽  
Gabriella D’Angelo ◽  
Caterina Cuppari ◽  
Erika Cusumano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Sequences ◽  
Allergic Diseases ◽  
Atopic Diseases ◽  
Cumulative Stress ◽  
Inducible Genes ◽  
The Relationship ◽  
And Oxidative Stress ◽  
Epigenetic Pattern

Although extensive epidemiological and laboratory studies have been performed to identify the environmental and immunological causes of atopy, genetic predisposition seems to be the biggest risk factor for allergic diseases. The onset of atopic diseases may be the result of heritable changes of gene expression, without any alteration in DNA sequences occurring in response to early environmental stimuli. Findings suggest that the establishment of a peculiar epigenetic pattern may also be generated by oxidative stress (OS) and perpetuated by the activation of OS-related genes. Analyzing the role of maternal and neonatal oxidative stress and oxidative stress-inducible genes, the purpose of this review was to summarize what is known about the relationship between maternal and neonatal OS-related genes and the development of atopic diseases.

scholarly journals Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes

2020 ◽  
Vol 21 (10) ◽  
pp. 3653
Author(s):  
Sara Cheleschi ◽  
Marcella Barbarino ◽  
Ines Gallo ◽  
Sara Tenti ◽  
Maria Bottaro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Hydrostatic Pressure ◽  
B Cell Lymphoma ◽  
Type Ii Collagen ◽  
Mrna Levels ◽  
Osteoarthritic Chondrocytes ◽  
The Relationship ◽  
And Oxidative Stress

Hydrostatic pressure (HP) modulates chondrocytes metabolism, however, its ability to regulate oxidative stress and microRNAs (miRNA) has not been clarified. The aim of this study was to investigate the role of miR-34a, miR-146a, and miR-181a as possible mediators of HP effects on oxidative stress in human osteoarthritis (OA) chondrocytes. Chondrocytes were exposed to cyclic low HP (1–5 MPa) and continuous static HP (10 MPa) for 3~h. Metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5, type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma 2 (BCL2) were evaluated by quantitative real-time polymerase chain reaction qRT-PCR, apoptosis and reactive oxygen species ROS production by cytometry, and β-catenin by immunofluorescence. The relationship among HP, the studied miRNA, and oxidative stress was assessed by transfection with miRNA specific inhibitors. Low cyclical HP significantly reduced apoptosis, the gene expression of MMP-13, ADAMTS5, miRNA, the production of superoxide anion, and mRNA levels of antioxidant enzymes. Conversely, an increased Col2a1 and BCL2 genes was observed. β-catenin protein expression was reduced in cells exposed to HP 1–5 MPa. Opposite results were obtained following continuous static HP application. Finally, miRNA silencing enhanced low HP and suppressed continuous HP-induced effects. Our data suggest miRNA as one of the mechanisms by which HP regulates chondrocyte metabolism and oxidative stress, via Wnt/β-catenin pathway.

scholarly journals Oxidative Stress and Bipolar Mood Disorder: An Important Yet Ambiguous Relationship

2022 ◽  
Author(s):  
Sara Rahsepar ◽  
Amirhooshang Mohammadpour
Keyword(s):  
Oxidative Stress ◽  
Bipolar Disorder ◽  
Thiobarbituric Acid ◽  
Bipolar Mood Disorder ◽  
Oxidative Markers ◽  
Stress Oxidative ◽  
Bipolar Patients ◽  
The Relationship ◽  
And Oxidative Stress

Bipolar disorder is a chronic psychological condition that disturbs many patients' lives around the world. The exact pathophysiology of bipolar disorder is yet unknown, but there are several hypotheses to explain this condition. One of the most challenging theories is the role of oxidative stress in the progression of bipolar disorder. Here, we conducted a narrative review to gather the studies that investigated the relationship between bipolar disorder and oxidative stress. We searched PubMed, Scopus, Web of science, and google scholar databases using the following keywords: “bipolar disorder,” “oxidative stress,” “oxidative markers,” and “bipolar patients.”     A majority of studies showed that oxidative markers such as Thiobarbituric acid reactive substances are significantly higher in bipolar patients compared to healthy subjects. Based on the included articles, bipolar disorder is associated with oxidative stress. Nevertheless, further well-established Cohorts are required to support these results.

scholarly journals The Role of Exosomal microRNAs and Oxidative Stress in Neurodegenerative Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Xiaoyu Wang ◽  
Yunxiang Zhou ◽  
Qiannan Gao ◽  
Dongnan Ping ◽  
Yali Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Cell Communication ◽  
Irreversible Damage ◽  
Exosomal Mirnas ◽  
A Cell ◽  
Physiological Pathways ◽  
The Relationship ◽  
And Oxidative Stress

Neurodegenerative diseases including Alzheimer’s disease and Parkinson’s disease are aging-associated diseases with irreversible damage of brain tissue. Oxidative stress is commonly detected in neurodegenerative diseases and related to neuronal injury and pathological progress. Exosome, one of the extracellular vesicles, is demonstrated to carry microRNAs (miRNAs) and build up a cell-cell communication in neurons. Recent research has found that exosomal miRNAs regulate the activity of multiple physiological pathways, including the oxidative stress response, in neurodegenerative diseases. Here, we review the role of exosomal miRNAs and oxidative stress in neurodegenerative diseases. Firstly, we explore the relationship between oxidative stress and neurodegenerative diseases. Secondly, we introduce the characteristics of exosomes and roles of exosome-related miRNAs. Thirdly, we summarized the crosstalk between exosomal miRNAs and oxidative stress in neurodegenerative diseases. Fourthly, we discuss the potential of exosomes to be a biomarker in neurodegenerative diseases. Finally, we summarize the advantages of exosome-based delivery and present situation of research on exosome-based delivery of therapeutic miRNA. Our work is aimed at probing and reinforcing the recognition of the pathomechanism of neurodegenerative diseases and providing the basis for novel strategies of clinical diagnosis and treatment.

Role of oxidative stress in the pathogenesis of postmenopausal osteoporosis (literature review)

2020 ◽  
pp. 29-42
Author(s):  
S. V. Bulgakova ◽  
A. V. Melikova
Keyword(s):  
Oxidative Stress ◽  
Literature Review ◽  
Postmenopausal Osteoporosis ◽  
Redox Homeostasis ◽  
Large Body ◽  
World Population ◽  
Social Significance ◽  
The Relationship ◽  
And Oxidative Stress

Postmenopausal osteoporosis is a disease of great medical and social significance for the world population. At the same time, the underlying pathogenesis of this pathology is not fully understood. A large body of research suggests that endocrine changes associated with postmenopause can lead to disruption of redox homeostasis and oxidative stress that affects bone metabolism. This literature review analyzes the relationship between hypoestrogenemia, oxidative stress and postmenopausal osteoporosis, as well as methods for the prevention and treatment of these conditions.

scholarly journals The Relationship between the Soluble Receptor for Advanced Glycation End Products and Oxidative Stress in Patients with Palmoplantar Warts

Medicina ◽  
2019 ◽  
Vol 55 (10) ◽  
pp. 706 ◽  
Author(s):  
Cristina Iulia Mitran ◽  
Ilinca Nicolae ◽  
Mircea Tampa ◽  
Madalina Irina Mitran ◽  
Constantin Caruntu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Serum Levels ◽  
Soluble Receptor ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
The Relationship ◽  
And Oxidative Stress ◽  
Inflammation Parameters

Background and objectives: Warts are the most common lesions caused by human papillomavirus (HPV). Recent research suggests that oxidative stress and inflammation are involved in the pathogenesis of HPV-related lesions. It has been shown that the soluble receptor for advanced glycation end products (sRAGE) may act as a protective factor against the deleterious effects of inflammation and oxidative stress, two interconnected processes. However, in HPV infection, the role of sRAGE, constitutively expressed in the skin, has not been investigated in previous studies. Materials and Methods: In order to analyze the role of sRAGE in warts, we investigated the link between sRAGE and the inflammatory response on one hand, and the relationship between sRAGE and the total oxidant/antioxidant status (TOS/TAS) on the other hand, in both patients with palmoplantar warts (n = 24) and healthy subjects as controls (n = 28). Results: Compared to the control group, our results showed that patients with warts had lower levels of sRAGE (1036.50 ± 207.60 pg/mL vs. 1215.32 ± 266.12 pg/mL, p < 0.05), higher serum levels of TOS (3.17 ± 0.27 vs. 2.93 ± 0.22 µmol H2O2 Eq/L, p < 0.01), lower serum levels of TAS (1.85 ± 0.12 vs. 2.03 ± 0.14 µmol Trolox Eq/L, p < 0.01) and minor variations of the inflammation parameters (high sensitivity-CRP, interleukin-6, fibrinogen, and erythrocyte sedimentation rate). Moreover, in patients with warts, sRAGE positively correlated with TAS (r = 0.43, p < 0.05), negatively correlated with TOS (r = −0.90, p < 0.01), and there was no significant correlation with inflammation parameters. There were no significant differences regarding the studied parameters between groups when we stratified the patients according to the number of the lesions and disease duration. Conclusions: Our results suggest that sRAGE acts as a negative regulator of oxidative stress and could represent a mediator involved in the development of warts. However, we consider that the level of sRAGE cannot be used as a biomarker for the severity of warts. To the best of our knowledge, this is the first study to demonstrate that sRAGE could be involved in HPV pathogenesis and represent a marker of oxidative stress in patients with warts.

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

The Concomitance of Hypertension and Diabetes Exacerbating Retinopathy: The Role of Inflammation and Oxidative Stress.

2013 ◽  
Vol 8 (4) ◽  
pp. 266-277 ◽  
Author(s):  
Diego Duarte ◽  
Kamila Silva ◽  
Mariana Rosales ◽  
José Lopes de Faria ◽  
Jacqueline Lopes de Faria
Keyword(s):  
Oxidative Stress ◽  
And Oxidative Stress

scholarly journals Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 629
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Hugo Christian Monroy-Ramírez ◽  
Marina Galicia-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peroxisome Proliferator ◽  
White Adipocyte ◽  
Peroxisome Proliferator Activated Receptors ◽  
And Oxidative Stress

Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

scholarly journals Neuroprotective Metabolites of Hericium erinaceus Promote Neuro-Healthy Aging

2021 ◽  
Vol 22 (12) ◽  
pp. 6379
Author(s):  
Elisa Roda ◽  
Erica Cecilia Priori ◽  
Daniela Ratto ◽  
Fabrizio De Luca ◽  
Carmine Di Iorio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Healthy Aging ◽  
Molecular Layer ◽  
Dietary Supplementation ◽  
Purkinje Neurons ◽  
Geriatric Syndrome ◽  
Oral Supplementation ◽  
Erinacine A ◽  
And Oxidative Stress

Frailty is a geriatric syndrome associated with both locomotor and cognitive decline, typically linked to chronic systemic inflammation, i.e., inflammaging. In the current study, we investigated the effect of a two-month oral supplementation with standardized extracts of H. erinaceus, containing a known amount of Erinacine A, Hericenone C, Hericenone D, and L-ergothioneine, on locomotor frailty and cerebellum of aged mice. Locomotor performances were monitored comparing healthy aging and frail mice. Cerebellar volume and cytoarchitecture, together with inflammatory and oxidative stress pathways, were assessed focusing on senescent frail animals. H. erinaceus partially recovered the aged-related decline of locomotor performances. Histopathological analyses paralleled by immunocytochemical evaluation of specific molecules strengthened the neuroprotective role of H. erinaceus able to ameliorate cerebellar alterations, i.e., milder volume reduction, slighter molecular layer thickness decrease and minor percentage of shrunken Purkinje neurons, also diminishing inflammation and oxidative stress in frail mice while increasing a key longevity regulator and a neuroprotective molecule. Thus, our present findings demonstrated the efficacy of a non-pharmacological approach, based on the dietary supplementation using H. erinaceus extract, which represent a promising adjuvant therapy to be associated with conventional geriatric treatments.

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