scholarly journals An in vitro model of renal inflammation after ischemic oxidative stress injury: nephroprotective effects of a hyaluronan ester with butyric acid on mesangial cells

2017 ◽  
Vol Volume 10 ◽  
pp. 135-142
Author(s):  
Olga Baraldi ◽  
Francesca Bianchi ◽  
Viola Menghi ◽  
Andrea Angeletti ◽  
Anna Laura Croci Chiocchini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Butyric Acid ◽  
In Vitro Model ◽  
Mesangial Cells ◽  
Stress Injury ◽  
Renal Inflammation ◽  
Oxidative Stress Injury ◽  
Vitro Model

scholarly journals Protective Effects and Mechanisms of Recombinant Human Glutathione Peroxidase 4 on Isoproterenol-Induced Myocardial Ischemia Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Chang Liu ◽  
Bozhao Li ◽  
Qi Yan ◽  
Shaopeng Niu ◽  
Yiding Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Glutathione Peroxidase ◽  
In Vitro Model ◽  
Cardiomyocyte Apoptosis ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Vitro Model

Ischemic heart disease (IHD) is a cardiovascular disease with high fatality rate, and its pathogenesis is closely related to oxidative stress. Reactive oxygen species (ROS) in oxidative stress can lead to myocardial ischemia (MI) injury in many ways. Therefore, the application of antioxidants may be an effective way to prevent IHD. In recent years, glutathione peroxidase 4 (GPx4) has received increasing attention due to its antioxidant effect. In a previous study, we used the new chimeric tRNAUTuT6 to express highly active recombinant human GPx4 (rhGPx4) in amber-less Escherichia coli. In this study, we established an isoproterenol- (ISO-) induced MI injury model in rats and an in vitro model to research the protective effect and mechanism of rhGPx4 on MI injury. The results showed that rhGPx4 could reduce the area of myocardial infarction and ameliorate the pathological injury of heart tissue, significantly reduce ISO-induced abnormalities on electrocardiogram (ECG) and cardiac serum biomarkers, protect mitochondrial function, and attenuate cardiac oxidative stress injury. In an in vitro model, the results also confirmed that rhGPx4 could inhibit ISO-induced oxidative stress injury and cardiomyocyte apoptosis. The mechanism of action of rhGPx4 involves not only the inhibition of lipid peroxidation by eliminating ROS but also keeping a normal level of endogenous antioxidant enzymes by eliminating ROS, thereby preventing oxidative stress injury in cardiomyocytes. Additionally, rhGPx4 could inhibit cardiomyocyte apoptosis through a mitochondria-dependent pathway. In short, rhGPx4, a recombinant antioxidant enzyme, can play an important role in the prevention of IHD and may have great potential for application.

scholarly journals S-Carboxymethyl Cysteine Protects against Oxidative Stress and Mitochondrial Impairment in a Parkinson’s Disease In Vitro Model

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1467
Author(s):  
Mariano Catanesi ◽  
Laura Brandolini ◽  
Michele d’Angelo ◽  
Maria Grazia Tupone ◽  
Elisabetta Benedetti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Dopaminergic Neurons ◽  
In Vitro Model ◽  
Night Time ◽  
Stress Injury ◽  
Vitro Model

The mucolytic agent S-carboxymethylcysteine is widely used as an expectorant for the treatment of numerous respiratory disorders. The metabolic fate of S-carboxymethyl-L-cysteine is complex. Several clinical studies have demonstrated that the metabolism of this agent differs within the same individual, with sulfur oxygenated metabolites generated upon night-time administration. It has been indicated that this drug behaves like a free radical scavenger and that, in this regard, the sulfide is the active species with sulphoxide metabolites (already oxidized) being inactive. Consequently, a night-time consumption of the drug should be more effective upon daytime administration. Still, this diurnal variation in biotransformation (deactivation) is dependent on the genetic polymorphism on which relies the patient population capacities of S-carboxymethyl-L-cysteine sulphoxidation. It has been reported that those cohorts who are efficient sulfur oxidizers will generate inactive oxygenated metabolites. In contrast, those who have a relative deficiency in this mechanism will be subjected to the active sulfide for a more extended period. In this regard, it is noteworthy that 38–39% of Parkinson’s disease patients belong to the poor sulphoxide cohort, being exposed to higher levels of active sulfide, the active antioxidant metabolite of S-carboxymethyl-L-cysteine. Parkinson’s disease is a neurodegenerative disorder that affects predominately dopaminergic neurons. It has been demonstrated that oxidative stress and mitochondrial dysfunction play a crucial role in the degeneration of dopaminergic neurons. Based on this evidence, in this study, we evaluated the effects of S-carboxymethyl cysteine in an in vitro model of Parkinson’s disease in protecting against oxidative stress injury. The data obtained suggested that an S-carboxymethylcysteine-enriched diet could be beneficial during aging to protect neurons from oxidative imbalance and mitochondrial dysfunction, thus preventing the progression of neurodegenerative processes.

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.

scholarly journals Rhubarb-Aconite Decoction (RAD) Drug-Containing Serum Alleviated Endotoxin-Induced Oxidative Stress Injury and Inflammatory Response in Caco-2 Cells In Vitro

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xiao-hong Du ◽  
Qing-jun Chen ◽  
Jian-bo Song ◽  
Yan Xie ◽  
Yan Zhi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Calcium Ion ◽  
Lipid Peroxide ◽  
Intestinal Injury ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Stress Injury ◽  
Oxidative Stress Injury

Rhubarb-Aconite Decoction (RAD), a famous Chinese medicine prescription, has been widely used for treating intestinal injury. However, the effect of RAD on intestinal epithelial cells is unclear. The aim of this study was to investigate the effects of RAD drug-containing serum on the oxidative stress injury and inflammatory response induced by endotoxin (ET) in Caco-2 cells in vitro. Lipid peroxide malondialdehyde (MDA), lactate dehydrogenase (LDH), caspase-11, tumor necrosis factor-α(TNF-α), interleukin-3(IL-3), and cytokeratin (CK)18, adenosine triphosphate (ATP) activity, and intracellular free calcium ion levels were measured. The results showed that ET triggered the activation of caspase-11 and the massive release of TNF-α, increased the inhibitory rate of cell growth, MDA, and LDH expressions in Caco-2 cells. Moreover, RAD drug-containing serum could inhibit caspase-11 activation, decrease the release of TNF-α and IL-3, reduce intracellular free calcium ion, and enhance CK 18 expression and ATP activity. These novel findings demonstrated that ET-induced oxidative stress injury and inflammatory response of Caco-2 cells were improved by RAD drug-containing serum, indicating that RAD may be a good choice for the treatment of intestinal injury.

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

scholarly journals Evaluation of low-grade In Vitro Oxidative Stress in Goat Erythrocytes ‎Exposed to Hydrogen Peroxide and Dexamethasone ‎

2021 ◽  
Vol 18 (2) ◽  
pp. 33-37
Author(s):  
M. B. Monguno ◽  
E. S. Philip ◽  
I. C. Uku ◽  
I. O. Igbokwe
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
In Vitro Model ◽  
Sucrose Solution ◽  
Osmotic Fragility ◽  
Low Grade ◽  
Mean Values ◽  
Red Blood Cell Count ◽  
Vitro Model

Under conditions of oxidative stress, erythrocytes of goats could be predisposed to haemolysis. This study was aimed at evaluating the effect of oxidant exposure to goat erythrocytes using an in vitro model. Blood samples from 10 goats were incubated with 0.06 – 0.18 mM hydrogen peroxide (H2O2) either singly or in combination with 0.02 µM dexamethasone for 60 min, and erythrocyte parameters such as packed cell volume (PCV), red blood cell count (RBC), mean corpuscular volume (MCV) and percentage haemolysis in hypotonic sucrose solution (250 mOsmol/L) were determined thereafter. No significant changes in the mean values of all parameters were observed. The in vitro model indicated that erythrocyte parameters remained stable under low-grade oxidant exposure in goats. Therefore, plasma H2O2 concentration of ≤ 0.18 mM, whether in the presence or absence of 0.02 µM dexamethasone, may not induce apparent oxidative damage in goat erythrocytes that could be estimated by PCV, RBC, MCV and sucrose-based osmotic fragility at low hypotonicity.

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