scholarly journals Vitamin A pretreatment protects NO-induced bovine mammary epithelial cells from oxidative stress by modulating Nrf2 and NF-κB signaling pathways

2018 ◽  
Vol 96 (4) ◽  
pp. 1305-1316 ◽  
Author(s):  
H Y Shi ◽  
S M Yan ◽  
Y M Guo ◽  
B Q Zhang ◽  
X Y Guo ◽  
...  
Animals ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 842 ◽  
Author(s):  
Lingling Sun ◽  
Fang Wang ◽  
Zhaohai Wu ◽  
Lu Ma ◽  
Craig Baumrucker ◽  
...  

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.


2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Mingjiang Liu ◽  
Guoqing Fang ◽  
Shaojie Yin ◽  
Xin Zhao ◽  
Chi Zhang ◽  
...  

In our previous study, lipopolysaccharide (LPS) significantly reduced the cell viability of primary bovine mammary epithelial cells (bMEC) leading to cell apoptosis, which were prevented by caffeic acid (CA) through inhibiting NF-κB activation and reducing proinflammatory cytokine expression. While the underlying mechanism remains unclear, here, we determined that LPS induced the extensive microstructural damage of bMEC, especially the mitochondria and endoplasmic reticulum. Then, the obvious reduction of mitochondrial membrane potential and expression changes of apoptosis-associated proteins (Bcl-2, Bax, and casepase-3) indicated that apoptosis signaling through the mitochondria should be responsible for the cell viability decrease. Next, the high-throughput cDNA sequencing (RNA-Seq) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were employed to verify that the MAPK and JAK-STAT signaling pathways also were the principal targets of LPS. Following, the critical proteins (ERK, JNK, p38, and c-jun) of the MAPK signaling pathways were activated, and the release of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8) regulated by NF-κB and MAPKs was significantly increased, which can promote a cascade of inflammation that induces cell injury and apoptosis. Meanwhile, CA significantly inhibited the activation of MAPKs and the release of proinflammatory cytokines in a dose-dependent manner, which were similar to its effects on the NF-κB activation that we previously published. So we concluded that CA regulates the proteins located in the upstream of multiple cell signal pathways which can reduce the LPS-induced activation of NF-κB and MAPKs, thus weakening the inflammatory response and maintaining cell structure and function, which accordingly inhibit apoptosis.


2019 ◽  
Vol 10 (10) ◽  
pp. 6276-6285 ◽  
Author(s):  
Xudong Sun ◽  
Hongdou Jia ◽  
Qiushi Xu ◽  
Chenxu Zhao ◽  
Chuang Xu

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


Oncotarget ◽  
2017 ◽  
Vol 8 (19) ◽  
pp. 31938-31947 ◽  
Author(s):  
Muhammad Shahid ◽  
Jian Gao ◽  
Yanan Zhou ◽  
Gang Liu ◽  
Tariq Ali ◽  
...  

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