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.

scholarly journals Curcumin Alleviates LPS-Induced Oxidative Stress, Inflammation and Apoptosis in Bovine Mammary Epithelial Cells via the NFE2L2 Signaling Pathway

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 208
Author(s):  
Ruihua Li ◽  
Hengtong Fang ◽  
Jinglin Shen ◽  
Yongcheng Jin ◽  
Yun Zhao ◽  
...  
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Cell Damage ◽  
Animal Health ◽  
Nuclear Factor Κb ◽  
Mammary Epithelial ◽  
Related Factor ◽  
Nuclear Factor ◽  
Bovine Mammary Epithelial Cells

Lipopolysaccharide (LPS) is an endotoxin, which may cause immune response and inflammation of bovine mammary glands. Mastitis impairs animal health and results in economic loss. Curcumin (CUR) is a naturally occurring diketone compound, which has attracted widespread attention as a potential anti-inflammatory antioxidant. The purpose of this study is to investigate whether CUR can reduce the damage of bovine mammary epithelial cells (MAC-T) induced by LPS and its underlying molecular mechanism. The MAC-T cell line was treated with different concentrations of LPS and CUR for 24 h. The results showed that CUR rescued the decrease of MAC-T cell viability and cell damage induced by LPS. At the same time, 10 µM CUR and 100 µg/mL LPS were used to treat the cells in the follow-up study. The results showed CUR treatment reduced the accumulation of reactive oxygen species (ROS), the expression of inflammatory cytokines (tumor necrosis factor-a (TNF-α), interleukin-8 (IL-8), IL-6 and IL-1β) and the rate of apoptosis induced by LPS. These effects were associated with the activation of the nuclear factor E2-related factor 2 (NFE2L2)-antioxidant response element (ARE) pathway coupled with inactivation of the nuclear factor-κB (NF-κB) inflammatory and caspase/Bcl2 apoptotic pathways.

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.

scholarly journals 5-ALA Attenuates the Palmitic Acid-Induced ER Stress and Apoptosis in Bovine Mammary Epithelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1183
Author(s):  
Mst Mamuna Sharmin ◽  
Md Aminul Islam ◽  
Itsuki Yamamoto ◽  
Shin Taniguchi ◽  
Shinichi Yonekura
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Palmitic Acid ◽  
Er Stress ◽  
Aminolevulinic Acid ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Protective Effects ◽  
Bovine Mammary Epithelial Cells ◽  
Induced Apoptosis

The conservation of mammary gland physiology by maintaining the maximum number of mammary epithelial cells (MECs) is of the utmost importance for the optimum amount of milk production. In a state of negative energy balance, palmitic acid (PA) reduces the number of bovine MECs. However, there is no effective strategy against PA-induced apoptosis of MECs. In the present study, 5-aminolevulinic acid (5-ALA) was established as a remedial agent against PA-induced apoptosis of MAC-T cells (an established line of bovine MECs). In PA-treated cells, the apoptosis-related genes BCL2 and BAX were down- and upregulated, respectively. The elevated expression of major genes of the unfolded protein response (UPR), such as CHOP, a proapoptotic marker (C/EBP homologous protein), reduced the viability of PA-treated MAC-T cells. In contrast, 5-ALA pretreatment increased and decreased BCL2 and BAX expression, respectively. Moreover, cleaved caspase-3 protein expression was significantly reduced in the 5-ALA-pretreated group in comparison with the PA group. The downregulation of major UPR-related genes, including CHOP, extended the viability of MAC-T cells pretreated with 5-ALA and also reduced the enhanced intensity of the PA-induced expression of phospho-protein kinase R-like ER kinase. Moreover, the enhanced expression of HO-1 (antioxidant gene heme oxygenase) by 5-ALA reduced PA-induced oxidative stress (OxS). HO-1 is not only protective against OxS but also effective against ER stress. Collectively, these findings offer new insights into the protective effects of 5-ALA against PA-induced apoptosis of bovine MECs.

scholarly journals MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhuo-Ma Luoreng ◽  
Da-Wei Wei ◽  
Xing-Ping Wang
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Bovine Mammary Epithelial Cells ◽  
Tnf Α

AbstractMastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3′ untranslated region (3′ UTR) of the NKIRAS2, but not the 3′UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.

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.

scholarly journals Simultaneous lack of catalase and beta-toxin in Staphylococcus aureus leads to increased intracellular survival in macrophages and epithelial cells and to attenuated virulence in murine and ovine models

Microbiology ◽  
2009 ◽  
Vol 155 (5) ◽  
pp. 1505-1515 ◽  
Author(s):  
Susana Martínez-Pulgarín ◽  
Gustavo Domínguez-Bernal ◽  
José A. Orden ◽  
Ricardo de la Fuente
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Epithelial Cells ◽  
Virulence Factors ◽  
Mammary Epithelial Cells ◽  
Intracellular Survival ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Wide Range ◽  
Beta Toxin

Staphylococcus aureus produces a variety of virulence factors that allow it to cause a wide range of infections in humans and animals. In the latter, S. aureus is a leading cause of intramammary infections. The contribution of catalase (KatA), an enzyme implicated in oxidative stress resistance, and beta-toxin (Hlb), a haemolysin, to the pathogenesis of S. aureus is poorly characterized. To investigate the role of these enzymes as potential virulence factors in S. aureus, we examined the intracellular survival of ΔkatA, Δhlb and ΔkatA Δhlb mutants in murine macrophages (J774A.1) and bovine mammary epithelial cells (MAC-T), and their virulence in different murine and ovine models. Catalase was not required for the survival of S. aureus within either J774A.1 or MAC-T cells. However, it was necessary for the intracellular proliferation of the bacterium after invasion of MAC-T cells. In addition, catalase was not needed for the full virulence of S. aureus in mice. Deletion of the hlb gene had no effect on the intracellular survival of S. aureus in J774A.1 cells but did cause a slight increase in survival in MAC-T cells. Furthermore, like catalase, beta-toxin was not required for complete virulence of S. aureus in murine models. Unexpectedly, the ΔkatA Δhlb mutant showed a notably increased persistence in both cell lines, and was significantly less virulent for mice than were the wild-type strain and single mutants. Most interestingly, it was also markedly attenuated in intramammary and subcutaneous infections in ewes and lambs.

scholarly journals Effects of Chinese Propolis in Protecting Bovine Mammary Epithelial Cells against Mastitis Pathogens-Induced Cell Damage

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Kai Wang ◽  
Xiao-Lu Jin ◽  
Xiao-Ge Shen ◽  
Li-Ping Sun ◽  
Li-Ming Wu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Inflammatory Responses ◽  
Mammary Epithelial Cells ◽  
Cell Damage ◽  
Mammary Epithelial ◽  
Active Components ◽  
Antioxidant Genes ◽  
Bovine Mammary Epithelial Cells ◽  
Chinese Propolis

Chinese propolis (CP), an important hive product, can alleviate inflammatory responses. However, little is known regarding the potential of propolis treatment for mastitis control. To investigate the anti-inflammatory effects of CP on bovine mammary epithelial cells (MAC-T), we used a range of pathogens to induce cellular inflammatory damage. Cell viability was determined and expressions of inflammatory/antioxidant genes were measured. Using a cell-based reporter assay system, we evaluated CP and its primary constituents on the NF-κB and Nrf2-ARE transcription activation. MAC-T cells treated with bacterial endotoxin (lipopolysaccharide, LPS), heat-inactivatedEscherichia coli,andStaphylococcus aureusexhibited significant decreases in cell viability while TNF-αand lipoteichoic acid (LTA) did not. Pretreatment with CP prevented losses in cell viability associated with the addition of killed bacteria or bacterial endotoxins. There were also corresponding decreases in expressions of proinflammatory IL-6 and TNF-αmRNA. Compared with the mastitis challenged cells, enhanced expressions of antioxidant genes HO-1, Txnrd-1, and GCLM were observed in CP-treated cells. CP and its polyphenolic active components (primarily caffeic acid phenethyl ester and quercetin) had strong inhibitive effects against NF-κB activation and increased the transcriptional activity of Nrf2-ARE. These findings suggest that propolis may be valuable in the control of bovine mastitis.

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.

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