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 MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway

2019 ◽  
Vol 20 (20) ◽  
pp. 5200 ◽  
Author(s):  
Cheleschi ◽  
Gallo ◽  
Barbarino ◽  
Giannotti ◽  
Mondanelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Structural Damage ◽  
Cultured Cells ◽  
B Cell Lymphoma ◽  
Synovial Fibroblasts ◽  
Type Ii Collagen ◽  
Superoxide Production ◽  
Nuclear Factor ◽  
Regulated Gene Expression ◽  
And Oxidative Stress

Synovial membrane inflammation actively participate to structural damage during osteoarthritis (OA). Adipokines, miRNA, and oxidative stress contribute to synovitis and cartilage destruction in OA. We investigated the relationship between visfatin, resistin and miRNA in oxidative stress regulation, in human OA synovial fibroblasts. Cultured cells were treated with visfatin and resistin. After 24 h, we evaluated various pro-inflammatory cytokines, metalloproteinases (MMPs), type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma (BCL)2 by qRT-PCR, apoptosis and mitochondrial superoxide production by cytometry, p50 nuclear factor (NF)-κB by immunofluorescence. Synoviocytes were transfected with miRNA inhibitors and oxidative stress evaluation after adipokines stimulus was performed. The implication of NF-κB pathway was assessed by the use of a NF-κB inhibitor (BAY-11-7082). Visfatin and resistin significantly up-regulated gene expression of interleukin (IL)-1β, IL-6, IL-17, tumor necrosis factor (TNF)-α, MMP-1, MMP-13 and reduced Col2a1. Furthermore, adipokines induced apoptosis and superoxide production, the transcriptional levels of BCL2, superoxide dismutase (SOD)-2, catalase (CAT), nuclear factor erythroid 2 like 2 (NRF2), miR-34a, miR-146a, and miR-181a. MiRNA inhibitors counteracted adipokines modulation of oxidative stress. Visfatin and resistin effects were suppressed by BAY-11-7082. Our data suggest that miRNA may represent possible mediators of oxidative stress induced by visfatin and resistin via NF-κB pathway in human OA synoviocytes.

Antioxidant Treatment Reverses Organ Failure in Rat Model of Sepsis: Role of Antioxidant Enzymes Imbalance, Neutrophil Infiltration, and Oxidative Stress

2011 ◽  
Vol 167 (2) ◽  
pp. e307-e313 ◽  
Author(s):  
Michael Andrades ◽  
Cristiane Ritter ◽  
Marcos Roberto de Oliveira ◽  
Emílio L. Streck ◽  
José Cláudio Fonseca Moreira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Organ Failure ◽  
Rat Model ◽  
Neutrophil Infiltration ◽  
Antioxidant Treatment ◽  
And Oxidative Stress

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 “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 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.

scholarly journals Antiapoptotic and antioxidative effects of cerium oxide nanoparticles on the testicular tissues of streptozotocin-induced diabetic rats: An experimental study

2021 ◽  
Author(s):  
Torab Solgi ◽  
Iraj Amiri ◽  
Sara Soleimani Asl ◽  
Massoud Saidijam ◽  
Banafsheh Mirzaei Seresht ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
B Cell ◽  
Caspase 3 ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Male Rats ◽  
Mrna Levels ◽  
Mrna Ratio ◽  
And Oxidative Stress

Background: Cerium dioxide nanoparticles (CNPs) due to the antidiabetic and antioxidant activities are proposed for the treatment of oxidative stress-associated diseases. Objective: To examine the impact of CNPs on hyperglycemia-induced apoptosis and oxidative stress in the testis of diabetic rats. Materials and Methods: Twenty-four male rats were divided into four groups (n = 6/each) as diabetic rats, CNPs group, diabetic + CNPs rats, and controls. The control group was fed only mouse food and water. Rats became diabetic through receiving streptozotocin (STZ) 60 mg/kg. CNPs were given to the rats at a dose of 30 mg/kg daily for 2 wk. Malondialdehyde and total thiol group (TTG) levels were measured using spectrofluorometer. Expression of b-cell lymphoma protein 2-associated X protein (BAX) and b-cell lymphoma protein 2 (Bcl-2) were investigated using quantitative real-time polymerase chain reaction. Western blot analysis was used to examine caspase 3 protein levels. Results: The content of malondialdehyde significantly increased in the STZ-diabetic rats, while TTG levels demonstrated a remarkable decrease. Caspase-3, BAX, and BAX/Bcl-2 mRNA ratio raised significantly in the STZ-diabetic rats. On the other hand, Bcl-2 mRNA levels reduced in the testis of diabetic rats (p = 0.006). Intervention with CNPs caused a substantial increase in the TTG levels, while the malondialdehyde contents, caspase-3, BAX levels, as well as BAX/Bcl-2 mRNA ratio were considerably decreased following CNPs treatment. Administration of CNPs increased mRNA levels of Bcl-2 (p < 0.0001). Conclusion: CNPs treatment attenuates testicular apoptosis and oxidative stress induced by diabetes. This nanoparticle might be suggested for the treatment of diabetes-associated reproductive disorders. Key words: Apoptosis, Nanoceria, Diabetes, Oxidative stress, Testis.

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.

The effects of crocin (active contstituent of saffron) treatment on brain antioxidant enzyme mRNA levels in diabetic rats / Diyabetik ratlarda safranın aktif içeriği olan krosin tedavisinin beyindeki antioksidan enzimlerin mRNA seviyeleri üzerine etkisi

2016 ◽  
Vol 41 (2) ◽  
Author(s):  
Eyüp Altınöz ◽  
Cemal Ekici ◽  
Berna Özyazgan ◽  
Yılmaz Çiğremiş
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Mrna Expression ◽  
Antioxidant Enzyme ◽  
Diabetic Rats ◽  
Control Group ◽  
Mrna Levels ◽  
The Brain ◽  
And Oxidative Stress

AbstractObjective: The aim of the present study is to evaluate the effect of crocin on mRNA expression of antioxidant enzymes, SOD, CAT and GPX in the brain of the STZ induced diabetic rats.Methods: Thirty animals randomized in three groups containing ten animals in each group as follows; control (non-diabetic rats), DM (STZ-induced untreated diabetic rats), DM+crocin (STZ-induced diabetic rats treated with crocin,). Crocin was given at a dose of 20 mg/kg bw/day by gavage for 21 days.Results: STZ injection caused a significant increase in mRNA expression of antioxidant enzymes, SOD, CAT and GPX when compared to control group. Crocin given to diabetic rats significantly decreased mRNA expression of antioxidant enzymes, SOD, CAT and GPX when compared to DM group.Conclusion: The present study demonstrates that crocin can modulate mRNA expression of antioxidant enzymes, SOD, CAT and GPX and oxidative stress in the brain of the STZ induced diabetic rats.

scholarly journals Exploring the Crosstalk between Hydrostatic Pressure and Adipokines: An In Vitro Study on Human Osteoarthritic Chondrocytes

2021 ◽  
Vol 22 (5) ◽  
pp. 2745
Author(s):  
Sara Cheleschi ◽  
Sara Tenti ◽  
Marcella Barbarino ◽  
Stefano Giannotti ◽  
Francesca Bellisai ◽  
...  
Keyword(s):  
Gene Expression ◽  
Antioxidant Enzymes ◽  
Hydrostatic Pressure ◽  
Cyclin D1 ◽  
Mirna Gene ◽  
In Vitro Study ◽  
B Cell Lymphoma ◽  
Superoxide Anion Production

Obesity is a risk factor for osteoarthritis (OA) development and progression due to an altered biomechanical stress on cartilage and an increased release of inflammatory adipokines from adipose tissue. Evidence suggests an interplay between loading and adipokines in chondrocytes metabolism modulation. We investigated the role of loading, as hydrostatic pressure (HP), in regulating visfatin-induced effects in human OA chondrocytes. Chondrocytes were stimulated with visfatin (24 h) and exposed to high continuous HP (24 MPa, 3 h) in the presence of visfatin inhibitor (FK866, 4 h pre-incubation). Apoptosis and oxidative stress were detected by cytometry, B-cell lymphoma (BCL)2, metalloproteinases (MMPs), type II collagen (Col2a1), antioxidant enzymes, miRNA, cyclin D1 expressions by real-time PCR, and β-catenin protein by western blot. HP exposure or visfatin stimulus significantly induced apoptosis, superoxide anion production, and MMP-3, -13, antioxidant enzymes, and miRNA gene expression, while reducing Col2a1 and BCL2 mRNA. Both stimuli significantly reduced β-catenin protein and increased cyclin D1 gene expression. HP exposure exacerbated visfatin-induced effects, which were counteracted by FK866 pre-treatment. Our data underline the complex interplay between loading and visfatin in controlling chondrocytes’ metabolism, contributing to explaining the role of obesity in OA etiopathogenesis, and confirming the importance of controlling body weight for disease treatment.

Sign in / Sign up

Export Citation Format

Share Document