scholarly journals Effects of microRNA-208a on inflammation and oxidative stress in ketamine-induced cardiotoxicity through Notch/NF-κB signal pathways by CHD9

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Hongjie Yuan ◽  
Shibin Du ◽  
Youliang Deng ◽  
Xiaoqing Xu ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Model ◽  
Epigenetic Modification ◽  
Heart Cell ◽  
Signal Pathways ◽  
Over Expression ◽  
Potential Biomarker ◽  
Vitro Model ◽  
And Oxidative Stress

Abstract Background: MicroRNA can regulate gene expression, and participate in multiple vital activities, such as inflammation, oxidative stress epigenetic modification, cell proliferation, and apoptosis. It plays an important role in the genesis and development of cardiovascular disease. Objective: To assess the role of microRNA-208a in ketamine-induced cardiotoxicity. Methods: All rats were randomly selected into two groups: sham and model groups. After fixed, all rats in the model group was intraperitoneally (IP) injected with 100 mg/kg of ketamine. Heart samples were stained with HE assay. Total RNAs from serum were used to hybridize with the SurePrint G3 Rat Whole Genome GE 8×60 K Microarray G4858A platform. Results: In the rat model with ketamine-induced cardiotoxicity, microRNA-208a expression was increased. Then, over-expression of microRNA-208a increased inflammation and oxidative stress in vitro model. However, down-regulation of microRNA-208a decreased inflammation and oxidative stress in vitro model. Over-expression of microRNA-208a suppressed CHD9 and Notch1, and induced p65 protein expression in vitro model. Overexpression of CHD9 reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through Notch/p65 signal pathways. Notch1 activation reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through p65 signal pathways. Conclusion: MicroRNA-208a may be a potential biomarker for ketamine-induced cardiotoxicity through inflammation and oxidative stress by Notch/NF-κB signal pathways by CHD9.

scholarly journals Protector role of intraocular lenses under artificial light conditions

2021 ◽  
Author(s):  
Andrés Fernández-Vega Cueto ◽  
Susana del Olmo-Aguado ◽  
Eva García-Pérez ◽  
Ignacio Rodriguez-Uña ◽  
Luis Fernández-Vega Cueto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Model ◽  
In Vitro Study ◽  
Artificial Light ◽  
Protective Effects ◽  
Light Conditions ◽  
Blue Led ◽  
Vitro Model ◽  
And Oxidative Stress

Introduction: The aim of this work is to analyse, in an in vitro model, the possible protective effects of ultraviolet- (UV-) or UV/ blue-filtering intraocular lens (IOLs) under LED lighting conditions. Methods: 10 models of IOLs were evaluated. Light transmission spectrum was recorded from 300 to 800 nm, in steps of 1 nm. Photodamage in vitro model was induced in ARPE-19 cells by blue LED light (465-475 nm). Changes in cell viability and oxidative stress variables were studied to assess the protective effect of IOLs. Results: UV/blue-filtering IOLs models block blue light spectrum in different proportion and UV-filtering IOLs blocking wavelength below 400 nm. However, in vitro study under blue LED light exposure does not show protective effects related with mitochondrial dysfunction and oxidative stress of UV/blue-filtering IOLs. Conclusions: The current in vitro study suggest that UV/blue filtering IOLs are not useful in terms of photoprotection in artificial light conditions. The results obtained indicate that it is needed to give attention to other IOLs parameters besides the type of filter, as it seems they could have influence also protective role.

scholarly journals Estimation of the Genotoxicityof Hydrogen Peroxide and Antioxidant Actionof Halo Acid by the Method of Dna-Cometwith the Use of the Model of Transplantable Cell Cultures

2018 ◽  
pp. 40-43
Author(s):  
Olga Verle ◽  
Oleg Ostrovskiy ◽  
Valerian Verovskiy ◽  
Galina Dudchenko
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
In Vitro Model ◽  
Cell Damage ◽  
Protective Action ◽  
Genetic Material ◽  
Optimal Level ◽  
Pharmacological Agents ◽  
Vitro Model

In the framework of the study, the degree of defragmentation of DNA by the DNA-comet method is evaluated when exposed to the cell culture of hydrogen peroxide (H2O2), and an in vitro model is developed to evaluate the antioxidant activity of new pharmacological agents. The results of working with cell lines show that the percentage of damage to the genetic material of cells of intact samples does not greatly vary from the method of removing the cellular monolayer from the culture plastic. Concerning the effect of H2O2 as an inducer of oxidative stress on DNA cell damage, the optimal level of DNA defragmentation has been modeled for subsequent studies of the protective action of antioxidants.

Cpt1a promoted ROS-induced oxidative stress and inflammation in liver injury via the Nrf2/HO-1 and NLRP3 inflammasome signaling pathway

2020 ◽  
Author(s):  
Xigang Luo ◽  
Dapeng Sun ◽  
Yinxiang Wang ◽  
Fengxiang Zhang ◽  
Yi Wang
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Signaling Pathway ◽  
Nlrp3 Inflammasome ◽  
Receptor Protein ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Over Expression ◽  
Vitro Model

Various liver diseases caused by liver damage seriously affect people’s health. The purpose of this study was to clarify that the effects and mechanism of Carnitine palmitoyltransferase 1 (Cpt1a) on oxidative stress and inflammation in liver injury. It was found that the expression of Cpt1a mRNA was up-regulated in model mice of liver injury. So, over-expression of Cpt1a increased reactive oxygen species (ROS) production and malondialdehyde (MDA) levels, and reduced superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GSH-px) levels in vitro model of liver injury. It was also shown that over-expression of Cpt1a suppressed the Nuclear factor-erythroid-2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) signaling pathway. In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome signaling pathway.

scholarly journals 2-Hydroxy-(4-methylseleno)butanoic Acid Is Used by Intestinal Caco-2 Cells as a Source of Selenium and Protects against Oxidative Stress

2019 ◽  
Vol 149 (12) ◽  
pp. 2191-2198
Author(s):  
Joan Campo-Sabariz ◽  
David Moral-Anter ◽  
M Teresa Brufau ◽  
Mickael Briens ◽  
Eric Pinloche ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Model ◽  
Thioredoxin Reductase ◽  
Protein Carbonyl ◽  
Butanoic Acid ◽  
H2o2 Treatment ◽  
Vitro Model ◽  
Gpx Activity

ABSTRACT Background Selenium (Se) participates in different functions in humans and other animals through its incorporation into selenoproteins as selenocysteine. Inadequate dietary Se is considered a risk factor for several chronic diseases associated with oxidative stress. Objective The role of 2-hydroxy-(4-methylseleno)butanoic acid (HMSeBA), an organic form of Se used in animal nutrition, in supporting selenoprotein synthesis and protecting against oxidative stress was investigated in an in vitro model of intestinal Caco-2 cells. Methods Glutathione peroxidase (GPX) and thioredoxin reductase (TXNRD) activities, selenoprotein P1 protein (SELENOP) and gene (SELENOP) expression, and GPX1 and GPX2 gene expression were studied in Se-deprived (FBS removal) and further HMSeBA-supplemented (0.1–625 μM, 72 h) cultures. The effect of HMSeBA supplementation (12.5 and 625 μM, 24 h) on oxidative stress induced by H2O2 (1 mM) was evaluated by the production of reactive oxygen species (ROS), 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyl residues compared with a sodium selenite control (SS, 5 μM). Results Se deprivation induced a reduction (P < 0.05) in GPX activity (62%), GPX1 expression, and both SELENOP (33%) and SELENOP expression. In contrast, an increase (P < 0.05) in GPX2 expression and no effect in TXNRD activity (P = 0.09) were observed. HMSeBA supplementation increased (P < 0.05) GPX activity (12.5–625 μM, 1.68–1.82-fold) and SELENOP protein expression (250 and 625 μM, 1.87- and 2.04-fold). Moreover, HMSeBA supplementation increased (P < 0.05) GPX1 (12.5 and 625 μM), GPX2 (625 μM), and SELENOP (12.5 and 625 μM) expression. HMSeBA (625 μM) was capable of decreasing (P < 0.05) ROS (32%), 4-HNE adduct (49%), and protein carbonyl residue (75%) production after H2O2 treatment. Conclusion Caco-2 cells can use HMSeBA as an Se source for selenoprotein synthesis, resulting in protection against oxidative stress.

scholarly journals An Insight into Sargassum muticum Cytoprotective Mechanisms against Oxidative Stress on a Human Cell In Vitro Model

Marine Drugs ◽  
2017 ◽  
Vol 15 (11) ◽  
pp. 353 ◽  
Author(s):  
Susete Pinteus ◽  
Marco Lemos ◽  
Joana Silva ◽  
Celso Alves ◽  
Agnieszka Neugebauer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Cell ◽  
In Vitro Model ◽  
Sargassum Muticum ◽  
Vitro Model ◽  
Insight Into

scholarly journals Trolox and Ascorbic Acid Reduce Direct and Indirect Oxidative Stress in the IPEC-J2 Cells, an In Vitro Model for the Porcine Gastrointestinal Tract

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0120485 ◽  
Author(s):  
Hans Vergauwen ◽  
Bart Tambuyzer ◽  
Karen Jennes ◽  
Jeroen Degroote ◽  
Wei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Gastrointestinal Tract ◽  
In Vitro Model ◽  
Vitro Model
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