scholarly journals Contribution of S6K1/MAPK Signaling Pathways in the Response to Oxidative Stress: Activation of RSK and MSK by Hydrogen Peroxide

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e75523 ◽  
Author(s):  
Anna Siebel ◽  
Monica Cubillos-Rojas ◽  
Roberto Christ Santos ◽  
Taiane Schneider ◽  
Carla Denise Bonan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Stress Activation ◽  
Mapk Signaling Pathways

scholarly journals Correction: Contribution of S6K1/MAPK Signaling Pathways in the Response to Oxidative Stress: Activation of RSK and MSK by Hydrogen Peroxide

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
Author(s):  
Anna Siebel ◽  
Monica Cubillos-Rojas ◽  
Roberto Christ Santos ◽  
Taiane Schneider ◽  
Carla Denise Bonan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Stress Activation ◽  
Mapk Signaling Pathways

scholarly journals Activation of the NF-κB and MAPK Signaling Pathways Contributes to the Inflammatory Responses, but Not Cell Injury, in IPEC-1 Cells Challenged with Hydrogen Peroxide

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Kan Xiao ◽  
Congcong Liu ◽  
Zhixiao Tu ◽  
Qiao Xu ◽  
Shaokui Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathways ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Intestinal Cell ◽  
Ldh Activity ◽  
Junction Protein ◽  
Mapk Signaling Pathways

Oxidative stress can lead to intestinal cell injury as well as the induction of inflammation. It is not clear whether inflammation is an important factor leading to cell injury caused by oxidative stress. The purpose of this study was to investigate the role of inflammation in intestinal injury caused by hydrogen peroxide (H2O2). Our results revealed that H2O2 stimulation significantly decreased the viability of intestinal porcine epithelial cells (IPEC-1), increased lactate dehydrogenase (LDH) activity, and disrupted the distribution of the tight junction protein claudin-1. H2O2 significantly increased the mRNA expression of interleukin-6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). H2O2 stimulation also led to increased phosphorylation of p38 and jun N-terminal kinase (JNK), and p65 NF-κB protein translocation into the nucleus of IPEC-1 cells. Cells treated with the NF-κB inhibitor (BAY11-7082), the p38 inhibitor (SB202190), or the JNK inhibitor (PD98059) significantly decreased mRNA and protein expression of IL-6, IL-8, and TNF-α. However, treatment with mitogen-activated protein kinase (MAPK) or NF-κB inhibitors did not prevent the damage effect on cell viability, LDH activity, or the distribution of claudin-1 in cells challenged with H2O2. In summary, our data demonstrate that activation of the NF-κB and MAPK signaling pathways can contribute to the inflammatory response, but not cell injury, in IPEC-1 cells challenged with H2O2.

scholarly journals Myricetin Protects Cells against Oxidative Stress-Induced Apoptosis via Regulation of PI3K/Akt and MAPK Signaling Pathways

2010 ◽  
Vol 11 (11) ◽  
pp. 4348-4360 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Zhi Hong Wang ◽  
Rui Zhang ◽  
Mei Jing Piao ◽  
Ki Cheon Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Induced Apoptosis ◽  
Mapk Signaling Pathways

scholarly journals Weaning Induced Hepatic Oxidative Stress, Apoptosis, and Aminotransferases through MAPK Signaling Pathways in Piglets

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Zhen Luo ◽  
Wei Zhu ◽  
Qi Guo ◽  
Wenli Luo ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Redox Status ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Control Group ◽  
Hepatic Oxidative Stress ◽  
Mitogen Activated Protein ◽  
D 20 ◽  
Mapk Signaling Pathways

This study investigated the effects of weaning on the hepatic redox status, apoptosis, function, and the mitogen-activated protein kinase (MAPK) signaling pathways during the first week after weaning in piglets. A total of 12 litters of piglets were weaned at d 21 and divided into the weaning group (WG) and the control group (CG). Six piglets from each group were slaughtered at d 0 (d 20, referred to weaning), d 1, d 4, and d 7 after weaning. Results showed that weaning significantly increased the concentrations of hepatic free radicals H2O2and NO, malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG), while significantly decreasing the inhibitory hydroxyl ability (IHA) and glutathione peroxidase (GSH-Px), and altered the level of superoxide dismutase (SOD). The apoptosis results showed that weaning increased the concentrations of caspase-3, caspase-8, caspase-9 and the ratio of Bax/Bcl-2. In addition, aspartate aminotransferase transaminase (AST) and alanine aminotransferase (ALT) in liver homogenates increased after weaning. The phosphorylated JNK and ERK1/2 increased, while the activated p38 initially decreased and then increased. Our results suggested that weaning increased the hepatic oxidative stress and aminotransferases and initiated apoptosis, which may be related to the activated MAPK pathways in postweaning piglets.

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