Simultaneous miRNA and mRNA Transcriptome Profiling of Differentiating Equine Satellite Cells Treated with Gamma-Oryzanol and Exposed to Hydrogen Peroxide

Gamma-oryzanol (GO) is a popular supplement for performance horses, dogs, and humans. Previous studies indicated that GO supplementation decreases creatine kinase activity and lactate level after exercise and may affect oxidative stress in Thoroughbred horses. GO may change genes expression in equine satellite cells (ESC). The purpose of this study was to evaluate the effect of GO on miRNA, gene expression, oxidative stress, and cell damage and viability in differentiating ESC pretreated with hydrogen peroxide (H2O2). ESCs were obtained from a young horse’s skeletal muscle. ESCs were pre-incubated with GO (24 h) and then exposed to H2O2 for one hour. For the microRNA and gene expression assessment, the microarray technique was used. Identified miRNAs and genes were validated using real time-quantitative polymerase chain reaction. Several tests related to cell viability, cell damage, and oxidative stress were performed. The microarray analysis revealed differences in 17 miRNAs and 202 genes between GO-treated and control ESC. The tests related to apoptosis, cell viability, and oxidative stress showed that GO affects these processes to varying degrees. Our results suggest that GO can change miRNA and gene expression and may impact the processes involved in tissue repairing after an injury.

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Hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in HepG2 cells

Current Nutraceuticals ◽

10.2174/2665978601999200807160528 ◽

2020 ◽

Vol 01 ◽

Author(s):

Ayşe Mine Yılmaz ◽

Gökhan Biçim ◽

Kübra Toprak ◽

Betül Karademir Yılmaz ◽

Irina Milisav ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Hydrogen Peroxide ◽

Cell Viability ◽

Hepg2 Cells ◽

Proteasome Activity ◽

Cell Cycle Phases ◽

Induced Changes ◽

And Oxidative Stress ◽

Quercetin Treatment

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

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ROLE OF PREGNAN-X-RECEPTOR IN CELL RESISTANCE TO NITROSATIVE AND OXIDATIVE STRESS

10.47501/978-5-6044060-1-4.47 ◽

2021 ◽

Author(s):

Yulia Abalenikhina ◽

◽

Elena A. Sudakova ◽

Pelageya Erokhina ◽

Aleksey Shchulkin ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Cell Viability ◽

Nitrosative Stress ◽

Pregnane X Receptor ◽

Cell Resistance ◽

Oxidative And Nitrosative Stress ◽

High Concentrations ◽

And Oxidative Stress

The article discusses the new role of pregnane X receptor (PXR) under conditions of oxidative and nitrosative stress. The results showed that the effect of hydrogen peroxide and S-nitrosoglu-tathione in high concentrations on Caco-2 cells leads to a decrease in cell viability, which is accompanied by an increase in the amount of PXR. These changes are offset by the addition of ketoconazole (inhibitor of PXR) to the medium.

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Adverse Effects of Nicotine and Immunosuppression on Proximal Tubular Epithelial Cell Viability, Tissue Repair and Oxidative Stress Gene Expression

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2009.03.003 ◽

2009 ◽

Vol 28 (6) ◽

pp. 612-620 ◽

Cited By ~ 8

Author(s):

Ashwani K. Khanna ◽

Jianping Xu ◽

Claudia Baquet ◽

Mandeep R. Mehra

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Epithelial Cell ◽

Adverse Effects ◽

Cell Viability ◽

Tissue Repair ◽

Tubular Epithelial Cell ◽

Proximal Tubular ◽

Stress Gene ◽

And Oxidative Stress

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Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134

Human & Experimental Toxicology ◽

10.1177/09603271211023784 ◽

2021 ◽

pp. 096032712110237

Author(s):

Y-J Li ◽

D-Z Zhang ◽

Y Xi ◽

C-A Wu

Keyword(s):

Oxidative Stress ◽

Cell Viability ◽

Pc12 Cells ◽

Cell Apoptosis ◽

Caspase 3 ◽

Cell Damage ◽

Annexin V ◽

Protective Effects ◽

Gene And Protein Expression ◽

And Oxidative Stress

Objective: To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells. Methods: Hydrogen peroxide (H2O2)-stimulated PC12 cells were divided into control, H2O2, DEX + H2O2, miR-NC/inhibitor + H2O2, and miR-NC/ mimic + DEX + H2O2 groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit. Results: DEX treatment decreased H2O2-elevated miR-134 expression. H2O2-induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H2O2-induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H2O2-induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic. Conclusion: DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H2O2-induced PC12 cells by inhibiting the expression of miR-134.

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Elevated extracellular CO2 level affects the adaptive transcriptional response and survival of human peripheral blood mononuclear cells toward hypoxia and oxidative stress

Medical Journal of Indonesia ◽

10.13181/mji.oa.203810 ◽

2021 ◽

Vol 30 (1) ◽

pp. 5-12

Author(s):

Septelia Inawati Wanandi ◽

Sekar Arumsari ◽

Edwin Afitriansyah ◽

Resda Akhra Syahrani ◽

Idham Rafly Dewantara ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Cell Viability ◽

Mononuclear Cells ◽

Human Peripheral Blood ◽

Transcriptional Response ◽

Peripheral Blood Mononuclear ◽

Blood Mononuclear Cells ◽

Co2 Level ◽

And Oxidative Stress

BACKGROUND High carbon dioxide (CO2) level from indoor environments, such as classrooms and offices, might cause sick building syndrome. Excessive indoor CO2 level increases CO2 level in the blood, and over-accumulation of CO2 induces an adaptive response that requires modulation of gene expression. This study aimed to investigate the adaptive transcriptional response toward hypoxia and oxidative stress in human peripheral blood mononuclear cells (PBMCs) exposed to elevated CO2 level in vitro and its association with cell viability. METHODS PBMCs were treated in 5% CO2 and 15% CO2, representatives a high CO₂ level condition for 24 and 48 hours. Extracellular pH (pHe) was measured with a pH meter. The levels of reactive oxygen species were determined by measuring superoxide and hydrogen peroxide with dihydroethidium and dichlorofluorescin-diacetate assay. The mRNA expression levels of hypoxia-inducible factor (HIF)-1α, HIF-2α, nuclear factor (NF)-κB, and manganese superoxide dismutase (MnSOD) were analyzed using a real-time reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell survival was determined by measuring cell viability. RESULTS pHe increased in 24 hours after 15% CO₂ treatment, and then decreased in 48 hours. Superoxide and hydrogen peroxide levels increased after the 24- and 48-hour of high CO₂ level condition. The expression levels of NF-κB, MnSOD, HIF-1α, and HIF-2α decreased in 24 hours and increased in 48 hours. The increased antioxidant mRNA expression in 48 hours showed that the PBMCs were responsive under high CO2 conditions. Elevated CO2 suppressed cell viability significantly in 48 hours. CONCLUSIONS After 48 hours of high CO₂ level condition, PBMCs showed an upregulation in genes related to hypoxia and oxidative stress to overcome the effects of CO2 elevation.

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A comparative analysis of cannabis and tobacco smoke exposure on human airway epithelial cell gene expression, immune phenotype, and response to formoterol and budesonide treatment

10.1101/516294 ◽

2019 ◽

Author(s):

Jennifer A. Aguiar ◽

Ryan D. Huff ◽

Wayne Tse ◽

Martin R. Stampfli ◽

Brendan J. McConkey ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Epithelial Cell ◽

Cell Viability ◽

Tobacco Smoke ◽

Barrier Function ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Airway Epithelial ◽

And Oxidative Stress

AbstractGlobal recreational cannabis use is a potentially important public health issue that would benefit from experimental evidence to inform policy, regulations, and individual user practices. Comparative analyses between cannabis and tobacco smoke, the latter long reported to have negative impacts on respiratory health, may help provide context and provide clinically relevant evidence.To address this unmet need we performed a comparative study between cannabis and tobacco smoke exposure in the Calu-3 human airway epithelial cells using concentration-response and pharmacological intervention study designs with outcome measurements of cell viability, epithelial cell barrier function, cytokine profile, and transcriptomics.Our results demonstrate that cannabis smoke exposure reduces epithelial cell barrier function without impacting cell viability, accompanied by a cytokine profile associated with inflammation (elevated IL-6 and IL-8), barrier repair (elevated TGF-α and PDGF-AA) and suppressed antiviral immunity (decreased IP-10 and RANTES). Transcriptomic analyses revealed a cannabis smoke induced signature associated with suppressed antiviral genes and induction of oncogenic and oxidative stress pathways. Similar trends were observed for tobacco smoke exposure. A formoterol/budesonide intervention was unable to prevent cannabis smoke-induced reductions in antiviral pathways or normalize induction of oncogenic and oxidative stress responses.Our results show striking similarities between cannabis and tobacco smoke exposure on impairing barrier function, suppressing antiviral pathways, potentiating of pro-inflammatory mediators, and inducing oncogenic and oxidative stress gene expression signatures. Furthermore, we demonstrate that an intervention with formoterol and budesonide is unable to completely normalized cannabisinduced responses. Collectively our data suggest that cannabis smoke exposure is not innocuous and may possess many of the deleterious properties of tobacco smoke, warranting additional studies to support public policy, government regulations, and individual user practices.

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FAM3A Protects HT22 Cells Against Hydrogen Peroxide-Induced Oxidative Stress Through Activation of PI3K/Akt but not MEK/ERK Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000438512 ◽

2015 ◽

Vol 37 (4) ◽

pp. 1431-1441 ◽

Cited By ~ 20

Author(s):

Qing Song ◽

Wen-Li Gou ◽

Rong Zhang

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Lipid Peroxidation ◽

Cell Viability ◽

Cell Damage ◽

Ros Generation ◽

Erk Pathway ◽

Protective Effects ◽

Ht22 Cells ◽

Ldh Release

Background/Aims: Oxidative stress-induced cell damage is involved in many neurological diseases. FAM3A is the first member of family with sequence similarity 3 (FAM3) gene family and its biological function remains largely unknown. Methods: This study aimed to determine its role in hydrogen peroxide (H2O2) induced injury in neuronal HT22 cells. The protective effects were measured by cell viability, lactate dehydrogenase (LDH) release and apoptosis, and oxidative stress was assayed by reactive oxygen species (ROS) generation, ATP synthesis and lipid peroxidation. By using selective inhibitors, the involvement of PI3K/Akt and MEK/ERK pathways were also investigated. Results: The results of fluorescence staining revealed that H2O2 significantly decreased the expression of FAM3A protein, which was shown to be subcellularly located in mitochondria. Up-regulation of FAM3A by lentivirus transfection markedly increased cell viability and decreased LDH release after H2O2 treatment. The anti-apoptotic activity of FAM3A was demonstrated by the reduced mitochondrial cytochrome c release, decreased activation of caspase-3 and the results of flow cytometry. Overexpression of FAM3A attenuated intracellular ROS generation and loss of ATP production induced by H2O2, and subsequently inhibited lipid peroxidation. In addition, overexpression of FAM3A significantly increased the activation of Akt and ERK in H2O2 injured HT22 cells. By using Akt and ERK specific inhibitors, we found that inhibition of PI3K/Akt, but not MEK/ERK pathway, partially prevented FAM3A-induced protection against H2O2. Conclusion: These results suggest that FAM3A has protective effects against H2O2-induced oxidative stress by reducing ROS accumulation and apoptosis, and these protective effects are dependent on the activation of PI3K/Akt pathway.

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Targeting ROS/NF-κB sigaling pathway by the seedless black Vitis vinifera polyphenols in CCl4-intoxicated kidney, lung, brain, and spleen in rats

Scientific Reports ◽

10.1038/s41598-021-96008-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Noha H. Habashy ◽

Ahmad S. Kodous ◽

Marwa M. Abu-Serie

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Vitis Vinifera ◽

Rat Kidney ◽

Environmental Pollutant ◽

Enhancing Effect ◽

Tnf Α ◽

Cox 2 ◽

Histopathological Studies ◽

And Oxidative Stress

AbstractCarbon tetrachloride (CCl4) is an abundant environmental pollutant that can generate free radicals and induce oxidative stress in different human and animal organs like the kidney, lung, brain, and spleen, causing toxicity. The present study evaluated the alleviative mechanism of the isolated polyphenolic fraction from seedless (pulp and skin) black Vitis vinifera (VVPF) on systemic oxidative and necroinflammatory stress in CCl4-intoxicated rats. Here, we found that the administration of VVPF to CCl4-intoxicated rats for ten days was obviously ameliorated the CCl4-induced systemic elevation in ROS, NO and TBARS levels, as well as MPO activity. Also, it upregulated the cellular activities of the enzymatic (SOD, and GPx) and non-enzymatic (TAC and GSH) antioxidants. Furthermore, the gene expression of the ROS-related necroinflammatory mediators (NF-κB, iNOS, COX-2, and TNF-α) in the kidney, brain, and spleen, as well as IL-1β, and IL-8 in the lung were greatly restored. The histopathological studies confirmed these biochemical results and showed a noticeable enhancing effect in the architecture of the studied organs after VVPF intake. Thus, this study indicated that VVPF had an alleviative effect on CCl4-induced necroinflammation and oxidative stress in rat kidney, lung, brain, and spleen via controlling the ROS/NF-κB pathway.

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