PEP-1–SIRT2 inhibits inflammatory response and oxidative stress-induced cell death via expression of antioxidant enzymes in murine macrophages

2013 ◽  
Vol 63 ◽  
pp. 432-445 ◽  
Author(s):  
Mi Jin Kim ◽  
Dae Won Kim ◽  
Jung Hwan Park ◽  
Sang Jin Kim ◽  
Chi Hern Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Antioxidant Enzymes ◽  
Inflammatory Response ◽  
Murine Macrophages ◽  
And Oxidative Stress

scholarly journals Energy Drink Administration in Combination with Alcohol Causes an Inflammatory Response and Oxidative Stress in the Hippocampus and Temporal Cortex of Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Alfonso Díaz ◽  
Samuel Treviño ◽  
Jorge Guevara ◽  
Guadalupe Muñoz-Arenas ◽  
Eduardo Brambila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Inflammatory Response ◽  
Temporal Cortex ◽  
Energy Drink ◽  
Brain Regions ◽  
Adult Rats ◽  
Mechanisms Of Toxicity ◽  
The Brain ◽  
And Oxidative Stress

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use of these psychoactive substances in combination with alcohol can trigger an oxidative and inflammatory response. These processes are regulated by both a reactive astrogliosis and an increase of proinflammatory cytokines such as IL-1β, TNF-α, and iNOS, causing cell death (apoptosis) at the central and peripheral nervous systems. Currently, mechanisms of toxicity caused by mixing alcohol and ED in the brain are not well known. In this study, we evaluated the effect of chronic alcohol consumption in combination with ED on inflammatory response and oxidative stress in the temporal cortex (TCx) and hippocampus (Hp) of adult rats (90 days old). Our results demonstrated that consuming a mixture of alcohol and ED for 60 days induced an increase in reactive gliosis, IL-1β, TNF-α, iNOS, reactive oxygen species, lipid peroxidation, and nitric oxide, in the TCx and Hp. We also found immunoreactivity to caspase-3 and a decrease of synaptophysin in the same brain regions. The results suggested that chronic consumption of alcohol in combination with ED causes an inflammatory response and oxidative stress, which induced cell death via apoptosis in the TCx and Hp of the adult rats.

Exogenous 24-Epibrassinolide stimulates root protection, and leaf antioxidant enzymes in rice plants lead stressed: Central roles to minimize Pb content and oxidative stress

2021 ◽  
pp. 116992
Author(s):  
Flávia Raphaela Carvalho Miranda Guedes ◽  
Camille Ferreira Maia ◽  
Breno Ricardo Serrão da Silva ◽  
Bruno Lemos Batista ◽  
Mohammed Nasser Alyemeni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Rice Plants ◽  
Root Protection ◽  
And Oxidative Stress

scholarly journals Caspase-2 and oxidative stress underlie the immunogenic potential of high hydrostatic pressure-induced cancer cell death

2016 ◽  
Vol 6 (1) ◽  
pp. e1258505 ◽  
Author(s):  
Irena Moserova ◽  
Iva Truxova ◽  
Abhishek D. Garg ◽  
Jakub Tomala ◽  
Patrizia Agostinis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Hydrostatic Pressure ◽  
Cancer Cell ◽  
High Hydrostatic Pressure ◽  
Cancer Cell Death ◽  
Caspase 2 ◽  
And Oxidative Stress

Cyane-carvone, a Synthetic Derivative of Carvone, Inhibits Inflammatory Response by Reducing Cytokine Production and Oxidative Stress and Shows Antinociceptive Effect in Mice

Inflammation ◽  
2014 ◽  
Author(s):  
Thiago Henrique Costa Marques ◽  
Maria Leonildes Boavista Gomes Cast Marques ◽  
Jand-Venes R. Medeiros ◽  
Renan Oliveira Silva ◽  
André Luiz dos Reis Barbosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cytokine Production ◽  
Antinociceptive Effect ◽  
Synthetic Derivative ◽  
And Oxidative Stress

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

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