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

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.

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

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.0c07521 ◽

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

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Effects of Glucose and Insulin on Rat Apolipoprotein A-I Gene Expression

Journal of Biological Chemistry ◽

10.1074/jbc.273.30.18959 ◽

1998 ◽

Vol 273 (30) ◽

pp. 18959-18965 ◽

Cited By ~ 89

Author(s):

Koji Murao ◽

Yoshinaru Wada ◽

Takaaki Nakamura ◽

Anthony H. Taylor ◽

Arshag D. Mooradian ◽

...

Keyword(s):

Gene Expression ◽

Apolipoprotein A ◽

I Gene

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Simultaneous miRNA and mRNA Transcriptome Profiling of Differentiating Equine Satellite Cells Treated with Gamma-Oryzanol and Exposed to Hydrogen Peroxide

Nutrients ◽

10.3390/nu10121871 ◽

2018 ◽

Vol 10 (12) ◽

pp. 1871

Author(s):

Karolina Chodkowska ◽

Anna Ciecierska ◽

Kinga Majchrzak ◽

Piotr Ostaszewski ◽

Tomasz Sadkowski

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Hydrogen Peroxide ◽

Cell Viability ◽

Satellite Cells ◽

Cell Damage ◽

Quantitative Polymerase Chain Reaction ◽

Mirna Gene ◽

Gamma Oryzanol ◽

And Oxidative Stress

Gamma-oryzanol (GO) is a popular supplement for performance horses, dogs, and humans. Previous studies indicated that GO supplementation decreases creatine kinase activity and lactate level after exercise and may affect oxidative stress in Thoroughbred horses. GO may change genes expression in equine satellite cells (ESC). The purpose of this study was to evaluate the effect of GO on miRNA, gene expression, oxidative stress, and cell damage and viability in differentiating ESC pretreated with hydrogen peroxide (H2O2). ESCs were obtained from a young horse’s skeletal muscle. ESCs were pre-incubated with GO (24 h) and then exposed to H2O2 for one hour. For the microRNA and gene expression assessment, the microarray technique was used. Identified miRNAs and genes were validated using real time-quantitative polymerase chain reaction. Several tests related to cell viability, cell damage, and oxidative stress were performed. The microarray analysis revealed differences in 17 miRNAs and 202 genes between GO-treated and control ESC. The tests related to apoptosis, cell viability, and oxidative stress showed that GO affects these processes to varying degrees. Our results suggest that GO can change miRNA and gene expression and may impact the processes involved in tissue repairing after an injury.

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Adiponectin enhances apolipoprotein a-1 gene expression in HepG2 cells: The studying of AdipoR1 and AdipoR2-dependent signaling pathways

Atherosclerosis ◽

10.1016/j.atherosclerosis.2020.10.261 ◽

2020 ◽

Vol 315 ◽

pp. e85

Author(s):

D. Tanyanskiy ◽

V.S. Shavva ◽

E. Dizhe ◽

G. Oleinikova ◽

A.V. Lizunov ◽

...

Keyword(s):

Gene Expression ◽

Signaling Pathways ◽

Hepg2 Cells ◽

Apolipoprotein A

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Differential regulation of apolipoprotein A-I gene expression by vitamin D receptor modulators

Biochimica et Biophysica Acta (BBA) - General Subjects ◽

10.1016/j.bbagen.2007.11.008 ◽

2008 ◽

Vol 1780 (2) ◽

pp. 264-273 ◽

Cited By ~ 21

Author(s):

Kent R. Wehmeier ◽

Angela Mazza ◽

Sahar Hachem ◽

Ken Ligaray ◽

Arshag D. Mooradian ◽

...

Keyword(s):

Gene Expression ◽

Vitamin D ◽

Vitamin D Receptor ◽

Differential Regulation ◽

Apolipoprotein A ◽

Receptor Modulators ◽

I Gene

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Induction of apolipoprotein A-I gene expression by glucagon-like peptide-1 and exendin-4 in hepatocytes but not intestinal cells

Metabolism ◽

10.1016/j.metabol.2012.07.005 ◽

2013 ◽

Vol 62 (2) ◽

pp. 265-274 ◽

Cited By ~ 9

Author(s):

Joe M. Chehade ◽

Rosalyn Alcalde ◽

Emad Naem ◽

Arshag D. Mooradian ◽

Norman C.W. Wong ◽

...

Keyword(s):

Gene Expression ◽

Intestinal Cells ◽

Apolipoprotein A ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

I Gene

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

BioMed Research International ◽

10.1155/2018/3169431 ◽

2018 ◽

Vol 2018 ◽

pp. 1-14 ◽

Cited By ~ 6

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.

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