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 Dandelion Extract Alleviated Lipopolysaccharide-Induced Oxidative Stress through the Nrf2 Pathway in Bovine Mammary Epithelial Cells

Toxins ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 496 ◽  
Author(s):  
Yawang Sun ◽  
Yongjiang Wu ◽  
Zili Wang ◽  
Juncai Chen ◽  
You Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Epithelial Cell Line ◽  
Related Factor ◽  
Nrf2 Pathway ◽  
Bovine Mammary Epithelial Cells ◽  
Nrf2 Signaling Pathway

In practical dairy production, cows are frequently subjected to inflammatory diseases, such as high-grain diet-induced subacute ruminal acidosis (SARA) as well as mastitis and metritis. Under the circumstances, lipopolysaccharide (LPS) induces oxidative stress within the cow and in the mammary epithelial cells. It has implications in practical production to alleviate oxidative stress and to optimize the lactational function of the mammary epithelial cells. This study thus aimed to investigate the antioxidative effects of dandelion aqueous extract (DAE) on LPS-induced oxidative stress and the mechanism of DAE as an antioxidant to alleviate oxidative stress through the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in the bovine mammary epithelial cell line MAC-T cells. The cells were cultured for 48 h in six treatments including control (without LPS and DAE), LPS (100 ng/mL), DAE10 (100 ng/mL LPS and 10 μg/mL DAE), DAE50 (100 ng/mL LPS and 50 μg/mL DAE), DAE100 (100 ng/mL LPS and 100 μg/mL DAE), and DAE200 (100 ng/mL LPS and 200 μg/mL DAE), respectively. The results showed that cell viability was reduced by LPS, and the adverse effect of LPS was suppressed with the supplementation of DAE. Lipopolysaccharide-induced oxidative stress through enhancing reactive oxygen species (ROS) production, resulted in increases in oxidative damage marker concentrations, while 10 and 50 μg/mL DAE alleviated the LPS-induced oxidative stress via scavenging cellular ROS and improving antioxidant enzyme activity. The upregulation of antioxidative gene expression in DAE treatments was promoted through activating the Nrf2 signaling pathway, with DAE at a concentration of 50 μg/mL exhibiting the highest effect. Overall, DAE acted as an effective antioxidant to inhibit LPS-induced oxidative stress and as a potential inducer of the Nrf2 signaling pathway.

scholarly journals Metformin Inhibits Lipoteichoic Acid–Induced Oxidative Stress and Inflammation Through AMPK/NRF2/NF-κB Signaling Pathway in Bovine Mammary Epithelial Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Abdelaziz Adam Idriss Arbab ◽  
Xubin Lu ◽  
Ismail Mohamed Abdalla ◽  
Amer Adam Idris ◽  
Zhi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Nuclear Localization ◽  
Mammary Epithelial Cells ◽  
Lipoteichoic Acid ◽  
Mammary Epithelial ◽  
Heme Oxygenase 1 ◽  
Nuclear Factor ◽  
Bovine Mammary Epithelial Cells

The objective of this research was to explore the effect of metformin on the lipoteichoic acid (LTA)–induced mastitis model using isolated primary bovine mammary epithelial cells (PBMECs). The PBMECs were exposed to either 3 mM metformin for 12 h as a metformin group (MET) or 100 μg/mL LTA for 6 h as LTA group (LTA). Cells pretreated with 3 mM metformin for 12 h followed by washing and 100 μg/mL LTA exposure for 6 h served as the MET + LTA group. Phosphate-buffered saline was added to cells as the control group. PBMECs pretreated with different metformin doses were analyzed by a flow cytometry (annexin V–fluorescein isothiocyanate assay) to detect the cell apoptotic rate. We performed quantitative reverse transcriptase–polymerase chain reaction and Western blot analysis to evaluate the inflammatory and oxidative responses to metformin and LTA by measuring cellular cytotoxicity, mRNA expression, and protein expression. Immunofluorescence was used to evaluate nuclear localization. The results showed that the gene expression of COX2, IL-1β, and IL-6 significantly increased in the cells challenged with LTA doses compared to control cells. In inflammatory PBMECs, metformin attenuated LTA-induced expression of inflammatory genes nuclear factor κB (NF-κB) p65, tumor necrosis factor α, cyclooxygenase 2, and interleukin 1β, as well as the nuclear localization and phosphorylation of NF-κBp65 protein, but increased the transcription of nuclear factor erythroid 2–related factor 2 (Nrf2) and Nrf2-targeted antioxidative genes heme oxygenase-1 (HO-1) and Gpx1, as well as the nuclear localization of HO-1 protein. Importantly, metformin-induced activation of Nrf2 is AMP-activated protein kinase (AMPK)–dependent; as metformin-pretreated PBMECs activated AMPK signaling via the upregulation of phosphorylated AMPK levels, cell pretreatment with metformin also reversed the translocation of Nrf2 that was LTA inhibited. This convergence between AMPK and Nrf2 pathways is essential for the anti-inflammatory effect of metformin in LTA-stimulated PBMECs. Altogether, our results indicate that metformin exerts anti-inflammation and oxidative stress through regulation of AMPK/Nrf2/NF-κB signaling pathway, which highlights the role of AMPK as a potential therapeutic strategy for treatment of bovine mastitis.

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 Comparison of Selenium Source in Preventing Oxidative Stress in Bovine Mammary Epithelial Cells

Animals ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 842 ◽  
Author(s):  
Lingling Sun ◽  
Fang Wang ◽  
Zhaohai Wu ◽  
Lu Ma ◽  
Craig Baumrucker ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Cell Damage ◽  
Antioxidant Response ◽  
Mammary Epithelial ◽  
Mrna Abundance ◽  
Bovine Mammary Epithelial Cells ◽  
Pre Treatment ◽  
Species Production

Oxidative stress can cause cell damage. Hydroxy-selenomethionine (HMSeBA) is an organic Se source with emerging antioxidant advantages. The objective of this study was to compare the effects of HMSeBA, selenomethionine (SeMet) and sodium selenite (SS) on the antioxidant response and the ability to resist oxidative stress in bovine mammary epithelial cells (BMEC). The BMEC were treated with 0 (Control), 20, 50, 100 and 150 nM HMSeBA, 100 nM SeMet and100 nM SS for 48 h. The results showed that HMSeBA and SeMet treatments had higher glutathione peroxidase (p < 0.01) and catalase (p = 0.01) activities and mRNA abundance of GPX3 (p = 0.02), but lower superoxide dismutase activity compared with SS (p = 0.04). The catalase activity (p < 0.05) and mRNA abundance of GPX3 (p = 0.04) changed in a quadratic manner with the increase of HMSeBA levels. To assess the potential protection of different Se sources against oxidative stress on BMEC, 0 or 50 μM H2O2 was added to BMEC culture for 3 h after Se pre-treatment for 48 h. The results showed that HMSeBA and SeMet, which did not differ (p > 0.05), but further decreased malondialdehyde and reactive oxygen species production compared with SS (p < 0.05). In conclusion, HMSeBA showed an enhanced cellular antioxidant status to resist oxidative damage induced by H2O2 when compared with SS, whereas the effects were similar to SeMet.

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