Upregulation Sestrin2 protects against hydrogen peroxide‐induced oxidative damage bovine mammary epithelial cells via a Keap1‐Nrf2/ARE pathway

2020 ◽  
Vol 236 (1) ◽  
pp. 392-404 ◽  
Author(s):  
Mengjiao Chen ◽  
Yumeng Xi ◽  
Kunlin Chen ◽  
Peng Xiao ◽  
Shujie Li ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells

scholarly journals Protection of bovine mammary epithelial cells from hydrogen peroxide-induced oxidative cell damage by selenium

2018 ◽  
Vol 63 (No. 3) ◽  
pp. 94-102
Author(s):  
Y.M. Guo ◽  
J. Gong ◽  
Y.G. Zheng ◽  
B.L. Shi ◽  
X.Y. Guo ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Mammary Epithelial Cells ◽  
Mapk Pathway ◽  
Mammary Epithelial ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Bovine Mammary Epithelial Cells

The uncontrolled release of arachidonic acid (ARA) and its metabolism by lipoxygenase (LOX) pathway can induce and aggravate cellular oxidative stress. Selenium (Se) is an integral part of some antioxidative selenoproteins and may protect cells from oxidative damage by modulating ARA release and metabolism. The present study aimed to investigate the protective response of Se against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative damage in bovine mammary epithelial cells (BMECs). The BMECs were incubated for 24 h in serum-free medium and then divided into four groups randomly. The cells in groups 1 and 2 were subsequently incubated for 30 h in serum-free medium containing 0 (control) and 50 nM Se (Se treatment group). The cells in groups 3 and 4 were incubated for 24 h in serum-free medium containing 0 and 50 nM Se, and then treated with 600 μM H<sub>2</sub>O<sub>2</sub> for 6 h (H<sub>2</sub>O<sub>2</sub> damage group and Se prevention group). The results showed that Se attenuated the H<sub>2</sub>O<sub>2</sub>-induced production of reactive oxygen species and the decrease of antioxidative enzymes as glutathione peroxidase (GPX), thioredoxin reductase (TrxR), selenoprotein P (SelP), superoxide dismutase, and catalase in BMECs. The preventive effects of Se on the decrease of selenoprotein activity were demonstrated further by the increase of mRNA expression for GPX1, TrxR1, and SelP, and protein expression for GPX1 and TrxR1. Pretreatment of cells with Se inhibited the H<sub>2</sub>O<sub>2</sub>-induced increase of mRNA expressions and activities for cytosolic phospholipase A2 and 5-lipoxygenase, ARA release, and 15-hydroperoxyeicosatetraenoic acid production. Se also blocked the H<sub>2</sub>O<sub>2</sub>-induced activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase but not that of extracellular signal-regulated kinase. These results suggested that Se may protect BMECs against H<sub>2</sub>O<sub>2</sub>-induced oxidative damage by increasing selenoproteins synthesis, inhibiting MAPK pathway, and then decreasing ARA release and its metabolism by LOX pathway.

Lycopene alleviates H2O2-induced oxidative stress, inflammation and apoptosis in bovine mammary epithelial cells via the NFE2L2 signaling pathway

2019 ◽  
Vol 10 (10) ◽  
pp. 6276-6285 ◽  
Author(s):  
Xudong Sun ◽  
Hongdou Jia ◽  
Qiushi Xu ◽  
Chenxu Zhao ◽  
Chuang Xu
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells

LYC against H2O2-induced oxidative damage in bMEC at least partly depended on activation of the NFE2L2 signaling pathway.

scholarly journals Retinoic acid attenuates oxidative injury in bovine mammary epithelial cells induced by hydrogen peroxide

2017 ◽  
Vol 62 (No. 12) ◽  
pp. 539-548
Author(s):  
L. Jin ◽  
S. Yan ◽  
B. Shi ◽  
H. Shi ◽  
X. Guo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hydrogen Peroxide ◽  
Arachidonic Acid ◽  
Retinoic Acid ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Oxidative Injury ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Pre Treatment

The objective of this study was to explore how retinoic acid (RA) attenuates oxidative injury induced by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) in bovine mammary epithelial cells (BMEC). Subconfluence BMEC were randomly divided into four groups with six replicates: the control group (incubated in serum-free medium without RA or H<sub>2</sub>O<sub>2 </sub>for 30 h), H<sub>2</sub>O<sub>2</sub> group (pre-incubated for 24 h without RA, then for another 6 h with 600 μM H<sub>2</sub>O<sub>2</sub>), RA group (incubated with 1 mg/ml RA for 30 h without H<sub>2</sub>O<sub>2</sub>), and RA + H<sub>2</sub>O<sub>2</sub> group (RA prevention group, pre-incubated with 1 mg/ml RA for 24 h and then for another 6 h with 600 mM H<sub>2</sub>O<sub>2</sub>). The results showed that the H<sub>2</sub>O<sub>2</sub> treatment significantly decreased several measured traits, including the cell viability, glutathione peroxidase (GPX) and thioredoxin reductase (TRXR) activities, selenoprotein P (SELP) content, catalase and superoxide dismutase activities, total antioxidant capacity, and GPX1, TRXR1, and SELP gene expression, as well as GPX1 and TRXR1 protein expression. H<sub>2</sub>O<sub>2</sub> treatment also increased the malondialdehyde and reactive oxygen species contents and induced a marked increase of several measured traits, including the arachidonic acid (ARA) concentration, cytosolic phospholipase A2 and 5-lipoxygenase gene expression and activity, and 15-hydroxy twenty-four arachidonic acid and hydroxy peroxide tetracosenic arachidonic acid contents. RA pre-treatment prevented corresponding increases in parameters related to ARA metabolism and increased the activity of TRXR. Moreover, RA pre-treatment attenuated the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase and effectively decreased the ARA content. These results suggest that RA protected BMEC from oxidative stress by elevating TRXR activity, which inhibited the MAPK signaling pathway and led to a decreased concentration of ARA.

scholarly journals Transcription factor EB (TFEB)-mediated autophagy protects bovine mammary epithelial cells against H2O2-induced oxidative damage in vitro

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xudong Sun ◽  
Renxu Chang ◽  
Yan Tang ◽  
Shengbin Luo ◽  
Chunhui Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Protein Abundance ◽  
Bovine Mammary Epithelial Cells ◽  
Ros Accumulation ◽  
Transcription Factor Eb

Abstract Background Bovine mammary epithelial cells after calving undergo serious metabolic challenges and oxidative stress both of which could compromise autophagy. Transcription factor EB (TFEB)-mediated autophagy is an important cytoprotective mechanism against oxidative stress. However, effects of TFEB-mediated autophagy on the oxidative stress of bovine mammary epithelial cells remain unknown. Therefore, the main aim of the study was to investigate the role of TFEB-mediated autophagy in bovine mammary epithelial cells experiencing oxidative stress. Results H2O2 challenge of the bovine mammary epithelial cell MAC-T increased protein abundance of LC3-II, increased number of autophagosomes and autolysosomes while decreased protein abundance of p62. Inhibition of autophagy via bafilomycin A1 aggravated H2O2-induced reactive oxygen species (ROS) accumulation and apoptosis in MAC-T cells. Furthermore, H2O2 treatment triggered the translocation of TFEB into the nucleus. Knockdown of TFEB by siRNA reversed the effect of H2O2 on protein abundance of LC3-II and p62 as well as the number of autophagosomes and autolysosomes. Overexpression of TFEB activated autophagy and attenuated H2O2-induced ROS accumulation. Furthermore, TFEB overexpression attenuated H2O2-induced apoptosis by downregulating the caspase apoptotic pathway. Conclusions Our results indicate that activation of TFEB mediated autophagy alleviates H2O2-induced oxidative damage by reducing ROS accumulation and inhibiting caspase-dependent apoptosis.

scholarly journals Protection of Bovine Mammary Epithelial Cells from Hydrogen Peroxide-Induced Oxidative Cell Damage by Resveratrol

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Xiaolu Jin ◽  
Kai Wang ◽  
Hongyun Liu ◽  
Fuliang Hu ◽  
Fengqi Zhao ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
T Cells ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mapk Pathway ◽  
Cell Damage ◽  
Cell Metabolism ◽  
Mammary Epithelial ◽  
Related Factor ◽  
Bovine Mammary Epithelial Cells

The mammary epithelial cells (MECs) of high-producing dairy cows are likely to be subject to oxidative stress (OS) due to the intensive cell metabolism. The objectives of this study were to investigate the cytoprotective effects of resveratrol against hydrogen peroxide- (H2O2-) induced OS in cultured bovine MECs (MAC-T). Pretreatment of MAC-T cells with resveratrol could rescue the decrease in cell viability and resulted in lower intracellular reactive oxygen species (ROS) accumulation after H2O2exposure. Resveratrol helped MAC-T cells to prevent H2O2-induced endoplasmic reticulum stress and mitochondria-related cell apoptosis. Moreover, resveratrol induced mRNA expression of multiple antioxidant defense genes in MAC-T cells under normal/oxidative conditions. Nuclear factor erythroid 2-related factor 2 (Nrf2) was required for the cytoprotective effects on MAC-T cells by resveratrol, as knockdown of Nrf2 significantly abolished resveratrol-induced cytoprotective effects against OS. In addition, by using selective inhibitors, we further confirmed that the induction of Nrf2 by resveratrol was mediated through the prolonged activation of PI3K/Akt and ERK/MAPK pathways but negatively regulated by p38/MAPK pathway. Overall, resveratrol has beneficial effects on bovine MECs redox balance and may be potentially used as a therapeutic medicine against oxidative insult in lactating animals.

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