Prevention of neuronal cell damage induced by oxidative stress in-vitro: effect of differentGinkgo bilobaextracts

2001 ◽  
Vol 53 (3) ◽  
pp. 387-392 ◽  
Author(s):  
Cristina Guidetti ◽  
Silvano Paracchini ◽  
Serena Lucchini ◽  
Maurizio Cambieri ◽  
Fulvio Marzatico
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Vitro Effect

scholarly journals Impact of Glucocorticoid on a Cellular Model of Parkinson’s Disease: Oxidative Stress and Mitochondrial Function

2021 ◽  
Vol 11 (8) ◽  
pp. 1106
Author(s):  
Silvia Claros ◽  
Antonio Gil ◽  
Mauro Martinelli ◽  
Nadia Valverde ◽  
Estrella Lara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Function ◽  
Cell Model ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Cellular Markers ◽  
The Impact

Stress seems to contribute to the neuropathology of Parkinson’s disease (PD), possibly by dysregulation of the hypothalamic–pituitary–adrenal axis. Oxidative distress and mitochondrial dysfunction are key factors involved in the pathophysiology of PD and neuronal glucocorticoid-induced toxicity. Animal PD models have been generated to study the effects of hormonal stress, but no in vitro model has yet been developed. Our aim was to examine the impact of corticosterone (CORT) administration on a dopaminergic neuronal cell model of PD induced by the neurotoxin MPP+, as a new combined PD model based on the marker of endocrine response to stress, CORT, and oxidative-mitochondrial damage. We determined the impact of CORT, MPP+ and their co-incubation on reactive oxygen species production (O2−•), oxidative stress cellular markers (advanced-oxidation protein products and total antioxidant status), mitochondrial function (mitochondrial membrane potential and mitochondrial oxygen consumption rate) and neurodegeneration (Fluoro-Jade staining). Accordingly, the administration of MPP+ or CORT individually led to cell damage compared to controls (p < 0.05), as determined by several methods, whereas their co-incubation produced strong cell damage (p < 0.05). The combined model described here could be appropriate for investigating neuropathological hallmarks and for evaluating potential new therapeutic tools for PD patients suffering mild to moderate emotional stress.

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 A novel mitochondrial enriched antioxidant protects neurons against acute oxidative stress

2017 ◽  
Author(s):  
Nicola J. Drummond ◽  
Nick O. Davies ◽  
Janet E. Lovett ◽  
Mark R. Miller ◽  
Graeme Cook ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Radical Scavenging ◽  
Head Group ◽  
Neural Cells ◽  
Zebrafish Model ◽  
Free System ◽  
Age Related

AbstractExcessive reactive oxygen species (ROS) can damage proteins, lipids, and DNA, which result in cell damage and death. The outcomes can be acute, as seen in stroke, or more chronic as observed in age-related diseases such as Parkinson’s disease. Here we investigate the antioxidant ability of a novel synthetic flavonoid, Proxison (7-decyl-3-hydroxy-2-(3,4,5-trihydroxyphenyl)-4-chromenone), using a range of in vitro and in vivo approaches. We show that, while it has radical scavenging ability on par with other flavonoids in a cell-free system, Proxison is orders of magnitude more potent than natural flavonoids at protecting neural cells against oxidative stress and is capable of rescuing damaged cells. The unique combination of a lipophilic hydrocarbon tail with a modified polyphenolic head group promotes efficient cellular uptake and mitochondrial localisation of Proxison. Importantly, in vivo administration of Proxison demonstrated effective and well tolerated neuroprotection against oxidative stress in a zebrafish model of dopaminergic neuronal loss.

In vitro effect of autologous platelet‐rich plasma on H 2 O 2 ‐induced oxidative stress in human spermatozoa

Andrology ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 191-200 ◽  
Author(s):  
R. Bader ◽  
J. N. Ibrahim ◽  
M. Moussa ◽  
A. Mourad ◽  
J. Azoury ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Platelet Rich Plasma ◽  
Human Spermatozoa ◽  
Autologous Platelet Rich Plasma ◽  
Vitro Effect ◽  
Autologous Platelet

In vitro effect of vanadyl sulfate on cultured primary astrocytes: cell viability and oxidative stress markers.

2020 ◽  
Vol 40 (6) ◽  
pp. 737-747
Author(s):  
Agnieszka Ścibior ◽  
Konrad A. Szychowski ◽  
Iwona Zwolak ◽  
Klaudia Dachowska ◽  
Jan Gmiński
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Vanadyl Sulfate ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Primary Astrocytes ◽  
Vitro Effect ◽  
And Oxidative Stress

scholarly journals Insights into Arbutin Effects on Bone Cells: Towards the Development of Antioxidant Titanium Implants

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 579 ◽  
Author(s):  
Maria A. Bonifacio ◽  
Giorgia Cerqueni ◽  
Stefania Cometa ◽  
Caterina Licini ◽  
Luigia Sabbatini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Cells ◽  
Cell Damage ◽  
Protective Role ◽  
Titanium Implants ◽  
Point Of View ◽  
Differentiation Markers ◽  
Scavenging Effect ◽  
High Viability

Arbutin is a plant-derived glycosylated hydroquinone with antioxidant features, exploited to combat cell damage induced by oxidative stress. The latter hinders the osseointegration of bone prostheses, leading to implant failure. Little is known about arbutin antioxidant effects on human osteoblasts, therefore, this study explores the in vitro protective role of arbutin on osteoblast-like cells (Saos-2) and periosteum-derived progenitor cells (PDPCs). Interestingly, cells exposed to oxidative stress were protected by arbutin, which preserved cell viability and differentiation. Starting from these encouraging results, an antioxidant coating loaded with arbutin was electrosynthesized on titanium. Therefore, for the first time, a polyacrylate-based system was designed to release the effective concentration of arbutin in situ. The innovative coating was characterized from the physico-chemical and morphological point of view to achieve an optimized system, which was in vitro tested with cells. Morpho-functional evaluations highlighted the high viability and good compatibility of the arbutin-loaded coating, which also promoted the expression of PDPC differentiation markers, even under oxidative stress. These results agreed with the coatings’ in vitro antioxidant activity, which showed a powerful scavenging effect against DPPH radicals. Taken together, the obtained results open intriguing opportunities for the further development of natural bioactive coatings for orthopedic titanium implants.

scholarly journals Inhibition of Oxidative Neurotoxicity and Scopolamine-Induced Memory Impairment by γ-Mangostin: In Vitro and In Vivo Evidence

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Youngmun Lee ◽  
Sunyoung Kim ◽  
Yeonsoo Oh ◽  
Young-Mi Kim ◽  
Young-Won Chin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Neuronal Damage ◽  
Biological Activities ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ros Generation ◽  
Garcinia Mangostana

Among a series of xanthones identified from mangosteen, the fruit of Garcinia mangostana L. (Guttifereae), α- and γ-mangostins are known to be major constituents exhibiting diverse biological activities. However, the effects of γ-mangostin on oxidative neurotoxicity and impaired memory are yet to be elucidated. In the present study, the protective effect of γ-mangostin on oxidative stress-induced neuronal cell death and its underlying action mechanism(s) were investigated and compared to that of α-mangostin using primary cultured rat cortical cells. In addition, the effect of orally administered γ-mangostin on scopolamine-induced memory impairment was evaluated in mice. We found that γ-mangostin exhibited prominent protection against H2O2- or xanthine/xanthine oxidase-induced oxidative neuronal death and inhibited reactive oxygen species (ROS) generation triggered by these oxidative insults. In contrast, α-mangostin had no effects on the oxidative neuronal damage or associated ROS production. We also found that γ-mangostin, not α-mangostin, significantly inhibited H2O2-induced DNA fragmentation and activation of caspases 3 and 9, demonstrating its antiapoptotic action. In addition, only γ-mangostin was found to effectively inhibit lipid peroxidation and DPPH radical formation, while both mangostins inhibited β-secretase activity. Furthermore, we observed that the oral administration of γ-mangostin at dosages of 10 and 30 mg/kg markedly improved scopolamine-induced memory impairment in mice. Collectively, these results provide both in vitro and in vivo evidences for the neuroprotective and memory enhancing effects of γ-mangostin. Multiple mechanisms underlying this neuroprotective action were suggested in this study. Based on our findings, γ-mangostin could serve as a potentially preferable candidate over α-mangostin in combatting oxidative stress-associated neurodegenerative diseases including Alzheimer’s disease.

In vitro effect of calcium dobesilate on oxidative/inflammatory stress in human varicose veins

2011 ◽  
Vol 26 (8) ◽  
pp. 332-337 ◽  
Author(s):  
O Alda ◽  
M S Valero ◽  
D Pereboom ◽  
P Serrano ◽  
J M Azcona ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Varicose Veins ◽  
Protective Action ◽  
Total Antioxidant Status ◽  
Pharmacokinetic Data ◽  
Calcium Dobesilate ◽  
Similar Action ◽  
Inflammatory Stress ◽  
Vitro Effect

Aim To determine whether calcium dobesilate can act in chronic venous insufficiency by similar antioxidant, anti-inflammatory mechanisms as in diabetic retinopathy. Methods Calcium dobesilate was tested in vitro for its protective action against oxidative/inflammatory stress in human varicose veins. Varicose greater saphenous veins were obtained from 14 patients (11 men, 3 women) aged 53–65 years. Oxidative stress was induced exogenously in the vein segments, with the phenazine methosulphate (PMS)/NADH couple. Total antioxidant status (TAS) and malondialdehyde (MDA) contents were used as markers of oxidative stress. Results Calcium dobesilate significantly prevented oxidative disturbances in the micromolar range. PMS/NADH-dependent TAS decrease was fully prevented with IC50 = 11.4 ± 2.3 µmol/L ( n = 6 veins), whereas MDA increase was fully prevented with IC50 = (102 ± −3) µmol/L ( n = 6 veins). Calcium dobesilate acted quali- and quantitatively like rutin, the reference compound. Comparison with pharmacokinetic data suggests that calcium dobesilate can act at therapeutic concentrations. Conclusion Calcium dobesilate protected human varicose veins against oxidative stress in vitro at levels that correspond to therapeutic concentrations. Further studies are required to investigate whether a similar action is found in varicose veins from patients orally treated with calcium dobesilate.

Effect of propofol on hypoxia re-oxygenation induced neuronal cell damage in vitro*

Anaesthesia ◽  
2012 ◽  
Vol 68 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Y. Huang ◽  
K. Zitta ◽  
B. Bein ◽  
J. Scholz ◽  
M. Steinfath ◽  
...  
Keyword(s):  
Cell Damage ◽  
Neuronal Cell

scholarly journals Antioxidant mimetics modulate oxidative stress and cellular signaling in airway epithelial cells infected with respiratory syncytial virus

2012 ◽  
Vol 303 (11) ◽  
pp. L991-L1000 ◽  
Author(s):  
Yashoda M. Hosakote ◽  
Narayana Komaravelli ◽  
Nicolas Mautemps ◽  
Tianshuang Liu ◽  
Roberto P. Garofalo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cell Damage ◽  
Cellular Signaling ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Proinflammatory Gene ◽  
Syncytial Virus ◽  
Proinflammatory Gene Expression

Respiratory syncytial virus (RSV) is one of the most common causes of bronchiolitis and pneumonia among infants and young children worldwide. In previous investigations, we have shown that RSV infection induces rapid generation of reactive oxygen species (ROS), which modulate viral-induced cellular signaling, and downregulation of antioxidant enzyme (AOE) expression, resulting in oxidative stress in vitro and in vivo, which plays a pathogenetic role in RSV-induced lung disease. In this study, we determined whether pharmacological intervention with synthetic catalytic scavengers could reduce RSV-induced proinflammatory gene expression and oxidative cell damage in an in vitro model of infection. Treatment of airway epithelial cells (AECs) with the salen-manganese complexes EUK-8 or EUK-189, which possess superoxide dismutase, catalase, and glutathione peroxidase activity, strongly reduced RSV-induced ROS formation by increasing cellular AOE enzymatic activity and levels of the lipid peroxidation products F2-8-isoprostane and malondialdehyde, which are markers of oxidative stress. Treatment of AECs with AOE mimetics also significantly inhibited RSV-induced cytokine and chemokine secretion and activation of the transcription factors nuclear factor-κB and interferon regulatory factor-3, which orchestrate proinflammatory gene expression. Both EUKs were able to reduce viral replication, when used at high doses. These results suggest that increasing antioxidant cellular capacities can significantly impact RSV-associated oxidative cell damage and cellular signaling and could represent a novel therapeutic approach in modulating virus-induced lung disease.

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