scholarly journals Protective effects of canolol against hydrogen peroxide-induced oxidative stress in AGS cells

RSC Advances ◽  
2017 ◽  
Vol 7 (68) ◽  
pp. 42826-42832 ◽  
Author(s):  
Ling Han ◽  
Xiaoyang Xia ◽  
Xia Xiang ◽  
Fenghong Huang ◽  
Zhen Zhang
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Phenolic Compound ◽  
Canola Oil ◽  
Protective Effects ◽  
Ags Cells

Canolol, a phenolic compound recently isolated from crude canola oil, effectively protected AGS cells against H2O2-induced oxidative stress.

scholarly journals Total Glucosides of Peony Protect Cardiomyocytes against Oxidative Stress and Inflammation by Reversing Mitochondrial Dynamics and Bioenergetics

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Mengmeng Wang ◽  
Qiang Li ◽  
Ying Zhang ◽  
Hao Liu
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lupus Erythematosus ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Bioenergetics ◽  
Protective Effects ◽  
Systemic Lupus ◽  
Regulatory Effects ◽  
Total Glucosides Of Peony

Total glucosides of peony (TGP) are used to treat rheumatoid arthritis and systemic lupus erythematosus. We explored the protective effects of TGP on cardiomyocyte oxidative stress and inflammation in the presence of hydrogen peroxide by focusing on mitochondrial dynamics and bioenergetics. Our study demonstrated that hydrogen peroxide significantly repressed cardiomyocyte viability and promoted cell apoptosis through induction of the mitochondrial death pathway. TGP treatment sustained cardiomyocyte viability, reduced cardiomyocyte apoptosis, and decreased inflammation and oxidative stress. Molecular investigation indicated that hydrogen peroxide caused mitochondrial dynamics disruption and bioenergetics reduction in cardiomyocytes, but this alteration could be normalized by TGP. We found that disruption of mitochondrial dynamics abolished the regulatory effects of TGP on mitochondrial bioenergetics; TGP modulated mitochondrial dynamics through the AMP-activated protein kinase (AMPK) pathway; and inhibition of AMPK alleviated the protective effects of TGP on mitochondria. Our results showed that TGP treatment reduces cardiomyocyte oxidative stress and inflammation in the presence of hydrogen peroxide by correcting mitochondrial dynamics and enhancing mitochondrial bioenergetics. Additionally, the regulatory effects of TGP on mitochondrial function seem to be mediated through the AMPK pathway. These findings are promising for myocardial injury in patients with rheumatoid arthritis and systemic lupus erythematosus.

scholarly journals Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide

2016 ◽  
Vol 17 (9) ◽  
pp. 692-702 ◽  
Author(s):  
Yun-zhi Ling ◽  
Xiao-hong Li ◽  
Li Yu ◽  
Ye Zhang ◽  
Qi-sheng Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effects ◽  
Primary Astrocytes

scholarly journals Tamoxifen inhibits mitochondrial membrane damage caused by disulfiram

2017 ◽  
Vol 95 (5) ◽  
pp. 556-562 ◽  
Author(s):  
Natalia Pavón ◽  
Mabel Buelna-Chontal ◽  
Francisco Correa ◽  
Belem Yoval-Sánchez ◽  
Javier Belmont ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cytochrome C ◽  
Mitochondrial Membrane ◽  
Membrane Damage ◽  
Mitochondrial Swelling ◽  
Protective Effects ◽  
Mitochondrial Enzyme ◽  
Inner Membrane ◽  
Antioxidant Molecule

In this work, we studied the protective effects of tamoxifen (TAM) on disulfiram (Dis)-induced mitochondrial membrane insult. The results indicate that TAM circumvents the inner membrane leakiness manifested as Ca2+ release, mitochondrial swelling, and collapse of the transmembrane electric gradient. Furthermore, it was found that TAM prevents inactivation of the mitochondrial enzyme aconitase and detachment of cytochrome c from the inner membrane. Interestingly, TAM also inhibited Dis-promoted generation of hydrogen peroxide. Given that TAM is an antioxidant molecule, it is plausible that its protection may be due to the inhibition of Dis-induced oxidative stress.

Protective effects of catalpol against hydrogen peroxide induced oxidative stress on preimplantation porcine embryos

2014 ◽  
Vol 31 ◽  
pp. S214
Author(s):  
Deog-Bon Koo ◽  
Yong-Hee Lee ◽  
Sung-Hun Min ◽  
Jin-Woo Kim ◽  
Jae-Hyun Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effects

scholarly journals Lipidomics reveal the protective effects of a vegetable-derived isothiocyanate against retinal degeneration

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1067 ◽  
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe
Keyword(s):  
Oxidative Stress ◽  
Mass Spectrometry ◽  
Hydrogen Peroxide ◽  
Fatty Acids ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Oxidative Damage ◽  
Disease Progression ◽  
Protective Effects ◽  
Retinal Cells

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.

scholarly journals Lingonberry anthocyanins protect cardiac cells from oxidative-stress-induced apoptosis

2017 ◽  
Vol 95 (8) ◽  
pp. 904-910 ◽  
Author(s):  
Cara K. Isaak ◽  
Jay C. Petkau ◽  
Heather Blewett ◽  
Karmin O ◽  
Yaw L. Siow
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Control Group ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Induced Apoptosis ◽  
Hoechst Staining

Lingonberry grown in northern Manitoba, Canada, contains exceptionally high levels of anthocyanins and other polyphenols. Previous studies from our lab have shown that lingonberry anthocyanins can protect H9c2 cells from ischemia–reperfusion injury and anthocyanin-rich diets have been shown to be associated with decreased cardiovascular disease and mortality. Oxidative stress can impair function and trigger apoptosis in cardiomyocytes. This study investigated the protective effects of physiologically relevant doses of lingonberry extracts and pure anthocyanins against hydrogen-peroxide-induced cell death. Apoptosis and necrosis were detected in H9c2 cells after hydrogen peroxide treatment via flow cytometry using FLICA 660 caspase 3/7 combined with YO-PRO-1 and then confirmed with Hoechst staining and fluorescence microscopy. Each of the 3 major anthocyanins found in lingonberry (cyanidin-3-galactoside, cyanidin-3-glucoside, and cyanidin-3-arabinoside) was protective against hydrogen-peroxide-induced apoptosis in H9c2 cells at 10 ng·mL−1 (20 nmol·L−1) and restored the number of viable cells to match the control group. A combination of the 3 anthocyanins was also protective and a lingonberry extract tested at 3 concentrations produced a dose-dependent protective effect. Lingonberry anthocyanins protected cardiac cells from oxidative-stress-induced apoptosis and may have cardioprotective effects as a dietary modification.

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