scholarly journals Pelargonidin Modulates Keap1/Nrf2 Pathway Gene Expression and Ameliorates Citrinin-Induced Oxidative Stress in HepG2 Cells

2017 ◽  
Vol 8 ◽  
Author(s):  
G. R. Sharath Babu ◽  
Tamatam Anand ◽  
N. Ilaiyaraja ◽  
Farhath Khanum ◽  
N. Gopalan
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hepg2 Cells ◽  
Nrf2 Pathway ◽  
Pathway Gene

scholarly journals Quantification and cytoprotection by vanillin, 4-methylguaiacol and 4-ethylguaiacol against AAPH-induced abnormal oxidative stress in HepG2 cells

RSC Advances ◽  
2018 ◽  
Vol 8 (62) ◽  
pp. 35474-35484 ◽  
Author(s):  
Dongrui Zhao ◽  
Dongmei Shi ◽  
Jinyuan Sun ◽  
Hehe Li ◽  
Mouming Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepg2 Cells ◽  
Nrf2 Pathway

Vanillin, 4-methylguaiacol, and 4-ethylguaiacol widely exist in Gujinggong Chinese baijiu and could protect HepG2 cells against oxidative stress via activating the Nrf2 pathway.

Sodium butyrate protects against oxidative stress in HepG2 cells through modulating Nrf2 pathway and mitochondrial function

2016 ◽  
Vol 73 (3) ◽  
pp. 405-414 ◽  
Author(s):  
Xingan Xing ◽  
Zheshu Jiang ◽  
Xue Tang ◽  
Panpan Wang ◽  
Yingrui Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sodium Butyrate ◽  
Mitochondrial Function ◽  
Hepg2 Cells ◽  
Nrf2 Pathway

scholarly journals Ellagic acid ameliorates oxidative stress and insulin resistance in high glucose-treated HepG2 cells via miR-223/keap1-Nrf2 pathway

2019 ◽  
Vol 110 ◽  
pp. 85-94 ◽  
Author(s):  
Xiaoqin Ding ◽  
Tunyu Jian ◽  
Yuexian Wu ◽  
Yuanyuan Zuo ◽  
Jiawei Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
High Glucose ◽  
Ellagic Acid ◽  
Hepg2 Cells ◽  
Nrf2 Pathway

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

scholarly journals Heat stress modulates polymorphonuclear cell response in early pregnancy cows: I. interferon pathway and oxidative stress

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257418
Author(s):  
Carolina dos Santos Amaral ◽  
Gabrielle Rebeca Everling Correa ◽  
Lady Katerine Serrano Mujica ◽  
Mariani Farias Fiorenza ◽  
Suzan Gonçalves Rosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Heat Stress ◽  
Early Pregnancy ◽  
Interferon Tau ◽  
Altered Expression ◽  
Stress Group ◽  
Pathway Gene ◽  
Interferon Pathway ◽  
And Oxidative Stress

One of the major causes of early pregnancy loss is heat stress. In ruminants, interferon tau (IFNT) is the embryo signal to the mother. Once the interferon signaling pathway is activated, it drives gene expression for interferon-stimulated genes (ISGs) and alters neutrophils responses. The aim of the present study was to evaluate interferon (IFN) pathway, ISGs and gene expression in polymorphonuclear leukocytes (PMN) and oxidative stress in dairy cows under heat stress. Pregnant cows had their estrous cycle synchronized and randomly assigned to a comfort or heat stress group. Blood samples were collected at artificial insemination (AI) and on Days 10, 14 and 18 following AI. Pregnant cows were pregnancy checked by ultrasound on Day 30 and confirmed on Day 60 post-AI. Results are presented as mean ± SEM. The corpus luteum (CL) diameter was not different between groups of pregnant cows; concentration of progesterone of pregnant cows on Day 18 following AI was greater in comfort group compared to heat stressed group. Comfort pregnant cows had higher expression of all analyzed genes from interferon pathway, except for IFNAR1, on both Days 14 and 18. Conversely, heat stressed cows did not show altered expression of IFNT pathway genes and ISGs between Days 10, 14, and 18 after AI. The oxidative stress, determined as malondialdehyde (MDA) levels, was greater in heat stress group on Days 10, 14 and 18, independent of pregnancy status. Heat stress negatively influences expression of ISGs, IFN pathway gene expression in neutrophils, and oxidative stress. Our data suggest that lower conception rates in cows under heat stress are multifactorial, with the association of interferon pathway activation and the unbalanced oxidative stress being main contributing factors.

scholarly journals Activation of the Keap1-Nrf2 pathway by specioside and the n-butanol extract from the inner bark of Tabebuia rosea (Bertol) DC

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 1262
Author(s):  
Sandra Catalina Garzón-Castaño ◽  
Francisco Javier Jiménez-González ◽  
Luz Angela Veloza ◽  
Juan Carlos Sepúlveda-Arias
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Hepg2 Cells ◽  
Radical Scavenging ◽  
Protective Effects ◽  
Nrf2 Pathway ◽  
Butanol Extract ◽  
Inner Bark ◽  
Mtt Method ◽  
Tabebuia Rosea

Background: A large number of chemical compounds exert their antioxidant effects by activation of key transcriptional regulatory mechanisms, such as the transcription factor Nrf2. The aim of this study was to evaluate the activation of the Keap1-Nrf2 pathway by both the n-butanol extract obtained from the inner bark of Tabebuia rosea (Bertol) DC and specioside isolated from this extract. Methods: The antioxidant activity of the extract and specioside isolated from the inner bark of T. rosea were evaluated using the oxygen radical absorbance capacity (ORAC) and the 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity (DPPH) techniques, whereas their effects on the viability of HepG2 cells was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. The effects of the compound and the extract on activating the Keap1-Nrf2 pathway were evaluated using a Nrf2 Transcription Factor Assay kit. Induction of the Nrf2-mediated antioxidant response genes HMOX-1 and NQO1 was evaluated by real-time PCR. The protective effects against H2O2-induced oxidative stress in HepG2 cells was determined as the percent protection using the MTT method. Results: Both the n-butanol extract and specioside exhibited activity at low concentrations without affecting cellular viability, since the cell viability was greater than 80% after 24 hours of exposure at each tested concentration. In addition, Nrf2 dissociated from Keap1 after treatment with the n-butanol extract at a concentration of 0.25 µg/mL after 4 hours of exposure. An increase in the Nrf2 level in the cytoplasm after 4 hours of exposure to 2 μM specioside was observed. Nrf2 levels stabilized in the nucleus 12 hours after stimulation with both specioside and the extract. After 6 hours of stimulation, both the extract and specioside induced the expression of HMOX-1 and NQO1. Conclusion: The n-butanol extract from the inner bark of T. rosea and specioside produced protective effects against H2O2-induced oxidative stress in HepG2 cells.

scholarly journals Activation of the Keap1-Nrf2 pathway by specioside and the n-butanol extract from the inner bark of Tabebuia rosea (Bertol) DC

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 1262
Author(s):  
Sandra Catalina Garzón-Castaño ◽  
Francisco Javier Jiménez-González ◽  
Luz Angela Veloza ◽  
Juan Carlos Sepúlveda-Arias
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Hepg2 Cells ◽  
Radical Scavenging ◽  
Protective Effects ◽  
Nrf2 Pathway ◽  
Butanol Extract ◽  
Inner Bark ◽  
Mtt Method ◽  
Tabebuia Rosea

Background: A large number of chemical compounds exert their antioxidant effects by activation of key transcriptional regulatory mechanisms, such as the transcription factor Nrf2. The aim of this study was to evaluate the activation of the Keap1-Nrf2 pathway by both the n-butanol extract obtained from the inner bark of Tabebuia rosea (Bertol) DC and specioside isolated from this extract. Methods: The antioxidant activity of the extract and specioside isolated from the inner bark of T. rosea were evaluated using the oxygen radical absorbance capacity (ORAC) and the 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity (DPPH) techniques, whereas their effects on the viability of HepG2 cells was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. The effects of the compound and the extract on activating the Keap1-Nrf2 pathway were evaluated using a Nrf2 Transcription Factor Assay kit. Induction of the Nrf2-mediated antioxidant response genes HMOX-1 and NQO1 was evaluated by real-time PCR. The protective effects against H2O2-induced oxidative stress in HepG2 cells was determined as the percent protection using the MTT method. Results: Both the n-butanol extract and specioside exhibited activity at low concentrations without affecting cellular viability, since the cell viability was greater than 80% after 24 hours of exposure at each tested concentration. In addition, Nrf2 dissociated from Keap1 after treatment with the n-butanol extract at a concentration of 0.25 µg/mL after 4 hours of exposure. An increase in the Nrf2 level in the cytoplasm after 4 hours of exposure to 2 μM specioside was observed. Nrf2 levels stabilized in the nucleus 12 hours after stimulation with both specioside and the extract. After 6 hours of stimulation, both the extract and specioside induced the expression of HMOX-1 and NQO1. Conclusion: The n-butanol extract from the inner bark of T. rosea and specioside produced protective effects against H2O2-induced oxidative stress in HepG2 cells.

scholarly journals 17β-Estradiol Promotes Apoptosis of HepG2 Cells Caused by Oxidative Stress by Increasing Foxo3a Phosphorylation

2021 ◽  
Vol 12 ◽  
Author(s):  
Yusheng Guo ◽  
Xiangsheng Cai ◽  
Hanwei Lu ◽  
Qiqi Li ◽  
Ying Zheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Superoxide Dismutase ◽  
Hepg2 Cells ◽  
Manganese Superoxide Dismutase ◽  
Manganese Superoxide ◽  
B Virus ◽  
17Β Estradiol ◽  
New Treatment

Liver cancer is associated with high mortality, particularly in patients infected with the hepatitis B virus. Treatment methods remain very limited. Here, we explored the effects of 17β-estradiol (E2) on apoptosis of various liver cell lines (LO2, HepG2, and HepG2.2.15 cells). Within a certain concentration range, 17β-estradiol induced oxidative stress and apoptosis of HepG2 cells, downregulated ERα-36 expression, and increased Akt and Foxo3a phosphorylation. p-Foxo3a became localized around the nucleus but did not enter the organelle. The levels of mRNAs encoding manganese superoxide dismutase (MnSOD) and catalase, to the promoters of which Foxo3a binds to trigger gene expression, were significantly reduced in HepG2 cells. 17β-estradiol had no obvious effects on LO2 or HepG2.2.15 cells. We speculate that 17β-estradiol may induce oxidative stress in HepG2 cells by increasing Foxo3a phosphorylation, thus promoting apoptosis. This may serve as a new treatment for hepatocellular carcinoma.

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