Methylated Metabolites of Chicoric Acid Ameliorate Hydrogen Peroxide (H2O2)-Induced Oxidative Stress in HepG2 Cells

2021 ◽  
Vol 69 (7) ◽  
pp. 2179-2189
Author(s):  
Xiaowen Chang ◽  
Shan Dong ◽  
Wenliang Bai ◽  
Yan Di ◽  
Ruijuan Gu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
Chicoric Acid

Hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in HepG2 cells

2020 ◽  
Vol 01 ◽  
Author(s):  
Ayşe Mine Yılmaz ◽  
Gökhan Biçim ◽  
Kübra Toprak ◽  
Betül Karademir Yılmaz ◽  
Irina Milisav ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Proteasome Activity ◽  
Cell Cycle Phases ◽  
Induced Changes ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

scholarly journals S-Allyl Cysteine Alleviates Hydrogen Peroxide Induced Oxidative Injury and Apoptosis through Upregulation of Akt/Nrf-2/HO-1 Signaling Pathway in HepG2 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Chitra Basu ◽  
Runa Sur
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Hepg2 Cells ◽  
Liver Diseases ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Cell Viability Assay

Hydrogen peroxide (H2O2) mediated oxidative stress leading to hepatocyte apoptosis plays a pivotal role in the pathophysiology of several chronic liver diseases. This study demonstrates that S-allyl cysteine (SAC) renders cytoprotective effects on H2O2 induced oxidative damage and apoptosis in HepG2 cells. Cell viability assay showed that SAC protected HepG2 cells from H2O2 induced cytotoxicity. Further, SAC treatment dose dependently inhibited H2O2 induced apoptosis via decreasing the Bax/Bcl-2 ratio, restoring mitochondrial membrane potential (∆Ψm), inhibiting mitochondrial cytochrome c release, and inhibiting proteolytic cleavage of caspase-3. SAC protected cells from H2O2 induced oxidative damage by inhibiting reactive oxygen species accumulation and lipid peroxidation. The mechanism underlying the antiapoptotic and antioxidative role of SAC is the induction of the heme oxygenase-1 (HO-1) gene in an NF-E2-related factor-2 (Nrf-2) and Akt dependent manner. Specifically SAC was found to induce the phosphorylation of Akt and enhance the nuclear localization of Nrf-2 in cells. Our results were further confirmed by specific HO-1 gene knockdown studies which clearly demonstrated that HO-1 induction indeed played a key role in SAC mediated inhibition of apoptosis and ROS production in HepG2 cells, thus suggesting a hepatoprotective role of SAC in combating oxidative stress mediated liver diseases.

Petroselinum sativum protects HepG2 cells from cytotoxicity and oxidative stress induced by hydrogen peroxide

2020 ◽  
Vol 47 (4) ◽  
pp. 2771-2780 ◽  
Author(s):  
Mai M. Al-Oqail ◽  
Nida N. Farshori ◽  
Ebtesam S. Al-Sheddi ◽  
Shaza M. Al-Massarani ◽  
Maqsood A. Siddiqui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
And Oxidative Stress

scholarly journals N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Jiying Jiang ◽  
Shuna Yu ◽  
Zhengchen Jiang ◽  
Cuihong Liang ◽  
Wenbo Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Hepg2 Cells ◽  
Morphological Changes ◽  
Mitochondrial Apoptosis ◽  
Sod Activity ◽  
Stress Injury ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway

Oxidative stress plays an important role in the pathogenesis of liver diseases. N-Acetyl-serotonin (NAS) has been reported to protect against oxidative damage, though the mechanisms by which NAS protects hepatocytes from oxidative stress remain unknown. To determine whether pretreatment with NAS could reduce hydrogen peroxide- (H2O2-) induced oxidative stress in HepG2 cells by inhibiting the mitochondrial apoptosis pathway, we investigated the H2O2-induced oxidative damage to HepG2 cells with or without NAS using MTT, Hoechst 33342, rhodamine 123, Terminal dUTP Nick End Labeling Assay (TUNEL), dihydrodichlorofluorescein (H2DCF), Annexin V and propidium iodide (PI) double staining, immunocytochemistry, and western blot. H2O2produced dramatic injuries in HepG2 cells, represented by classical morphological changes of apoptosis, increased levels of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), decreased activity of superoxide dismutase (SOD), and increased activities of caspase-9 and caspase-3, release of cytochrome c (Cyt-C) and apoptosis-inducing factor (AIF) from mitochondria, and loss of membrane potential (ΔΨm). NAS significantly inhibited H2O2-induced changes, indicating that it protected against H2O2-induced oxidative damage by reducing MDA levels and increasing SOD activity and that it protected the HepG2 cells from apoptosis through regulating the mitochondrial apoptosis pathway, involving inhibition of mitochondrial hyperpolarization, release of mitochondrial apoptogenic factors, and caspase activity.

scholarly journals Tea polyphenols ameliorate hydrogen peroxide- and constant darkness-triggered oxidative stress via modulating the Keap1/Nrf2 transcriptional signaling pathway in HepG2 cells and mice liver

RSC Advances ◽  
2017 ◽  
Vol 7 (51) ◽  
pp. 32198-32208 ◽  
Author(s):  
Guoyuan Qi ◽  
Yashi Mi ◽  
Rong Fan ◽  
Runnan Li ◽  
Yiwen Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathway ◽  
Hepg2 Cells ◽  
Tea Polyphenols ◽  
Constant Darkness ◽  
Mice Liver

Tea polyphenols alleviate oxidative stressviamodulating the Keap1/Nrf2 transcriptional signaling pathway in HepG2 cells and the liver of mice kept in constant darkness.

Effect of soybean peptides against hydrogen peroxide induced oxidative stress in HepG2 cells via Nrf2 signaling

2020 ◽  
Vol 11 (3) ◽  
pp. 2725-2737 ◽  
Author(s):  
Guofu Yi ◽  
Jalal ud Din ◽  
Fen Zhao ◽  
Xinqi Liu
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Activity ◽  
Hepg2 Cells ◽  
Soybean Protein ◽  
Protein Hydrolysates

The aim of this study was to determine the effects of soybean protein hydrolysates against intracellular antioxidant activity.

scholarly journals FOXO1 and LXRα downregulate the apolipoprotein A-I gene expression during hydrogen peroxide-induced oxidative stress in HepG2 cells

2016 ◽  
Vol 22 (1) ◽  
pp. 123-134 ◽  
Author(s):  
Vladimir S. Shavva ◽  
Alexandra M. Bogomolova ◽  
Artemy A. Nikitin ◽  
Ella B. Dizhe ◽  
Galina N. Oleinikova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
Apolipoprotein A ◽  
I Gene

Anti-genotoxic and cytoprotective effects of a multi-herbal extract against oxidative stress induced by hydrogen peroxide in HepG2 cells

2021 ◽  
Vol 140 ◽  
pp. 11-16
Author(s):  
Fatemeh Soltani ◽  
Omid Fakharzadeh Moghadam ◽  
Niloofar Nadalizadeh ◽  
Seyed Ahmad Emami ◽  
Behjat Javadi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
Herbal Extract
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