scholarly journals Protective Effect of Astaxanthin on Blue Light Light-Emitting Diode-Induced Retinal Cell Damage via Free Radical Scavenging and Activation of PI3K/Akt/Nrf2 Pathway in 661W Cell Model

Marine Drugs ◽  
2020 ◽  
Vol 18 (8) ◽  
pp. 387 ◽  
Author(s):  
Chao-Wen Lin ◽  
Chung-May Yang ◽  
Chang-Hao Yang
Keyword(s):  
Antioxidant Enzymes ◽  
Free Radical ◽  
Protective Effect ◽  
Blue Light ◽  
Nuclear Translocation ◽  
Light Exposure ◽  
Cell Damage ◽  
Radical Scavenging ◽  
Photoreceptor Cells ◽  
Light Emitting

Light-emitting diodes (LEDs) are widely used and energy-efficient light sources in modern life that emit higher levels of short-wavelength blue light. Excessive blue light exposure may damage the photoreceptor cells in our eyes. Astaxanthin, a xanthophyll that is abundantly available in seafood, is a potent free radical scavenger and anti-inflammatory agent. We used a 661W photoreceptor cell line to investigate the protective effect of astaxanthin on blue light LED-induced retinal injury. The cells were treated with various concentrations of astaxanthin and then exposed to blue light LED. Our results showed that pretreatment with astaxanthin inhibited blue light LED-induced cell apoptosis and prevented cell death. Moreover, the protective effect was concentration dependent. Astaxanthin suppressed the production of reactive oxygen species and oxidative stress biomarkers and diminished mitochondrial damage induced by blue light exposure. Western blot analysis confirmed that astaxanthin activated the PI3K/Akt pathway, induced the nuclear translocation of Nrf2, and increased the expression of phase II antioxidant enzymes. The expression of antioxidant enzymes and the suppression of apoptosis-related proteins eventually protected the 661W cells against blue light LED-induced cell damage. Thus, our results demonstrated that astaxanthin exerted a dose-dependent protective effect on photoreceptor cells against damage mediated by blue light LED exposure.

Exploring the Protective Potential of Carboxymethyl Terminalia catappa Polysaccharide on Blue Light Light-Emitting Diode Induced Corneal Damage

2020 ◽  
Vol 13 (4) ◽  
pp. 310-322 ◽  
Author(s):  
Lalit Chandel ◽  
Radhika Sharma ◽  
Vikas Rana
Keyword(s):  
Protective Effect ◽  
Blue Light ◽  
Light Emitting Diode ◽  
Radical Scavenging Activity ◽  
Protective Action ◽  
Radical Scavenging ◽  
Light Emitting ◽  
Terminalia Catappa ◽  
Structural Recovery ◽  
Corneal Damage

Background: Excessive blue light light-emitting diode (LED) exposure and consequent oxidative stress causes corneal damage and corneal injuries are the major problem arising these days due to excessive use of mobile phone, TV, environment pollution, etc. Objective: In the present investigation, the protectiveness of carboxymethyl Terminalia catappa (CTC) from blue light LED-induced corneal damage was explored. Methods: For this purpose, Terminalia catappa (TC) was functionalized by carboxymethylation and its structural modification was confirmed by spectral attributes. Further, the CTC protective eye drop formulations (0.025-1%, w/v) were prepared and evaluated for their capability of protection from blue light LEDinduced corneal damage as compared to CTC protective eye gel (1.25-7%, w/v). The findings pointed towards excellent protection of CTC gel formulations as compared to CTC eye drop formulations. In addition, the prepared optimized CTC gel had thixotropic behavior as evident from percentage structural recovery which was 1.75 fold higher than marketed formulation (I-Comfort, HPMC 2%, w/v). The safety and non-toxicity of CTC protective eye drop and gel were confirmed by HET-CAM test. Further, a rat eye model was implemented that mimic blue light light-emitting diode induced corneal damage in day to day life to assess the protective effect of CTC protective eye drop and gel. Results: The order of protectiveness of CTC formulations was found to be CTC protective eye gel (4%, w/v) (no corneal damage)>marketed eye gel (12.34% corneal damage)=CTC protective eye drop (0.75%, w/v) (17.48% corneal damage)> marketed eye drop (51% corneal damage). The mechanism behind the protective effect of CTC eye drop and gel was associated with good free radical scavenging activity and corneal adhesive property of CTC. It is established from the present work that, carboxymethyl Terminalia catappa has protective action against blue light light-emitting diode induced corneal damage.

scholarly journals Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

Free radical scavenging capacity and protective effect ofBacopa monniera L. on DNA damage

2003 ◽  
Vol 17 (8) ◽  
pp. 870-875 ◽  
Author(s):  
Alessandra Russo ◽  
Angelo A. Izzo ◽  
Francesca Borrelli ◽  
Marcella Renis ◽  
Angelo Vanella
Keyword(s):  
Dna Damage ◽  
Free Radical ◽  
Protective Effect ◽  
Radical Scavenging ◽  
Free Radical Scavenging ◽  
Radical Scavenging Capacity ◽  
Scavenging Capacity

l-carnitine protects human hepatocytes from oxidative stress-induced toxicity through Akt-mediated activation of Nrf2 signaling pathway

2016 ◽  
Vol 94 (5) ◽  
pp. 517-525 ◽  
Author(s):  
Jinlian Li ◽  
Yanli Zhang ◽  
Haiyun Luan ◽  
Xuehong Chen ◽  
Yantao Han ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Cell Damage ◽  
Binding Activity ◽  
Akt Pathway ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Akt Inhibitor ◽  
Nrf2 Signaling Pathway

In our previous study, l-carnitine was shown to have cytoprotective effect against hydrogen peroxide (H2O2)-induced injury in human normal HL7702 hepatocytes. The aim of this study was to investigate whether the protective effect of l-carnitine was associated with the nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) pathway. Our results showed that pretreatment with l-carnitine augmented Nrf2 nuclear translocation, DNA binding activity and heme oxygenase-1 (HO-1) expression in H2O2-treated HL7702 cells, although l-carnitine treatment alone had no effect on them. Analysis using Nrf2 siRNA demonstrated that Nrf2 activation was involved in l-carnitine-induced HO-1 expression. In addition, l-carnitine-mediated protection against H2O2 toxicity was abrogated by Nrf2 siRNA, indicating the important role of Nrf2 in l-carnitine-induced cytoprotection. Further experiments revealed that l-carnitine pretreatment enhanced the phosphorylation of Akt in H2O2-treated cells. Blocking Akt pathway with inhibitor partly abrogated the protective effect of l-carnitine. Moreover, our finding demonstrated that the induction of Nrf2 translocation and HO-1 expression by l-carnitine directly correlated with the Akt pathway because Akt inhibitor showed inhibitory effects on the Nrf2 translocation and HO-1 expression. Altogether, these results demonstrate that l-carnitine protects HL7702 cells against H2O2-induced cell damage through Akt-mediated activation of Nrf2 signaling pathway.

scholarly journals New 1,8-Naphthalimide Derivatives as Photoinitiators for Free-Radical Polymerization Upon Visible Light

Catalysts ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 637 ◽  
Author(s):  
Aude-Héloïse Bonardi ◽  
Soraya Zahouily ◽  
Céline Dietlin ◽  
Bernadette Graff ◽  
Fabrice Morlet-Savary ◽  
...  
Keyword(s):  
Free Radical ◽  
Visible Light ◽  
Radical Polymerization ◽  
Light Exposure ◽  
Free Radical Polymerization ◽  
Thermal Processes ◽  
Light Emitting ◽  
Chemical Mechanisms ◽  
Full Picture ◽  
Methacrylate Monomers

Photopolymerization processes, and especially those carried out under visible light, are more and more widespread for their multiple advantages compared to thermal processes. In the present paper, new 1,8-naphthalimide derivatives are proposed as photoinitiators for free-radical polymerization upon visible light exposure using light-emitting diodes (LEDs) at 395, 405, and 470 nm. These photoinitiators are used in combination with both iodonium salts and phosphine. The synthesis of these compounds as well as their excellent polymerization initiation ability for methacrylate monomers are presented in this article. A full picture of the involved chemical mechanisms is also provided thanks to photolysis, radical characterization, and redox measurements.

scholarly journals Free Radical–Mediated Cell Damage After Experimental Status Epilepticus in Hippocampal Slice Cultures

2002 ◽  
Vol 88 (6) ◽  
pp. 2909-2918 ◽  
Author(s):  
Richard Kovács ◽  
Sebastian Schuchmann ◽  
Siegrun Gabriel ◽  
Oliver Kann ◽  
Julianna Kardos ◽  
...  
Keyword(s):  
Free Radicals ◽  
Status Epilepticus ◽  
Free Radical ◽  
Hippocampal Slice ◽  
Cell Damage ◽  
Radical Scavenging ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Mitochondrial Depolarization ◽  
Hippocampal Slice Cultures

Generation of free radicals may have a key role in the nerve cell damage induced by prolonged or frequently recurring convulsions (status epilepticus). Mitochondrial function may also be altered due to production of free radicals during seizures. We therefore studied changes in field potentials (fp) together with measurements of extracellular, intracellular, and intramitochondrial calcium concentration ([Ca2+]e, [Ca2+]i, and [Ca2+]m, respectively), mitochondrial membrane potential (ΔΨ), NAD(P)H auto-fluorescence, and dihydroethidium (HEt) fluorescence in hippocampal slice cultures by means of simultaneous electrophysiological and microfluorimetric measurements. As reported previously, each seizure-like event (SLE) resulted in mitochondrial depolarization associated with a delayed rise in oxidation of HEt to ethidum, presumably indicating ROS production. We show here that repeated SLEs led to a decline in intracellular and intramitochondrial Ca2+ signals despite unaltered Ca2+ influx. Also, mitochondrial depolarization and the NAD(P)H signal became smaller during recurring SLEs. By contrast, the ethidium fluorescence rises remained constant or even increased from SLE to SLE. After about 15 SLEs, activity changed to continuous afterdischarges with steady depolarization of mitochondrial membranes. Staining with a cell death marker, propidium iodide, indicated widespread cell damage after 2 h of recurring SLEs. The free radical scavenger, α-tocopherol, protected the slice cultures against this damage and also reduced the ongoing impairment of NAD(P)H production. These findings suggest involvement of reactive oxygen species (ROS) of mitochondrial origin in the epileptic cell damage and that free radical scavenging may prevent status epilepticus–induced cell loss.

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