scholarly journals Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E2 Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 190 ◽  
Author(s):  
Jae Won Ha ◽  
Hyerim Song ◽  
Seong Su Hong ◽  
Yong Chool Boo
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Particulate Matter ◽  
Prostaglandin E2 ◽  
Pge2 Production ◽  
Ecklonia Cava ◽  
Epidermal Keratinocytes ◽  
Hacat Keratinocytes ◽  
Cox 2 ◽  
Cox 1

Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of E. cava extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of E. cava extract or dieckol and analyzed for their viability, prostaglandin E2 (PGE2) release, and gene expression of cyclooxygenase (COX)-1, COX-2, microsomal prostaglandin E2 synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E2 synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE2, and these changes were partially abrogated by E. cava extract. E. cava extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE2 production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that E. cava extract and dieckol alleviate airborne PM10-induced PGE2 production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus, E. cava extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM.

scholarly journals Induction of Cyclooxygenase-2 Gene in Pancreatic β-Cells by 12-Lipoxygenase Pathway Product 12-Hydroxyeicosatetraenoic Acid

2002 ◽  
Vol 16 (9) ◽  
pp. 2145-2154 ◽  
Author(s):  
Xiao Han ◽  
Songyuan Chen ◽  
Yujie Sun ◽  
Jerry L. Nadler ◽  
David Bleich
Keyword(s):  
Gene Expression ◽  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Pge2 Production ◽  
Hydroxyeicosatetraenoic Acid ◽  
Lipoxygenase Inhibitor ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Cox 2 ◽  
12 Lipoxygenase

Abstract Cyclooxygenase-2 (COX-2) gene and 12-lipoxygenase (12-LO) gene are preferentially expressed over other types of cyclooxygenase and lipoxygenase in pancreatic β-cells. Inhibition of either COX-2 or 12-LO can prevent cytokine-induced pancreatic β-cell dysfunction as defined by inhibition of glucose-stimulated insulin secretion. As cellular stress induces both genes and their respective end products in pancreatic β-cells, we evaluated the role of 12-hydroxyeicosatetraenoic acid (HETE) on COX-2 gene expression, protein expression, and prostaglandin E2 (PGE2) production. We demonstrate that 12-HETE significantly increases COX-2 gene expression and consequent product formation, whereas a closely related lipid, 15-HETE, does not. In addition, IL-1β-stimulated prostaglandin E2 production is completely inhibited by a preferential lipoxygenase inhibitor cinnaminyl-3,4-dihydroxy-α-cyanocinnamate. We then evaluated IL-1β-induced PGE2 production in islets purified from control C57BL/6 mice and 12-LO knockout mice lacking cytokine-inducible 12-HETE. IL-1β stimulated an 8-fold increase in PGE2 production in C57BL/6 islets but failed to stimulate PGE2 in 12-LO knockout islets. Addition of 12-HETE to 12-LO knockout islet cells produced a statistically significant rise in PGE2 production. Furthermore, 12-HETE, but not 15-HETE, stimulated COX-2 promoter and activator protein-1 binding activity. These data demonstrate that 12-HETE mediates cytokine-induced COX-2 gene transcription and resultant PGE2 production in pancreatic β-cells.

scholarly journals Targeting ROS/NF-κB sigaling pathway by the seedless black Vitis vinifera polyphenols in CCl4-intoxicated kidney, lung, brain, and spleen in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Noha H. Habashy ◽  
Ahmad S. Kodous ◽  
Marwa M. Abu-Serie
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Vitis Vinifera ◽  
Rat Kidney ◽  
Environmental Pollutant ◽  
Enhancing Effect ◽  
Tnf Α ◽  
Cox 2 ◽  
Histopathological Studies ◽  
And Oxidative Stress

AbstractCarbon tetrachloride (CCl4) is an abundant environmental pollutant that can generate free radicals and induce oxidative stress in different human and animal organs like the kidney, lung, brain, and spleen, causing toxicity. The present study evaluated the alleviative mechanism of the isolated polyphenolic fraction from seedless (pulp and skin) black Vitis vinifera (VVPF) on systemic oxidative and necroinflammatory stress in CCl4-intoxicated rats. Here, we found that the administration of VVPF to CCl4-intoxicated rats for ten days was obviously ameliorated the CCl4-induced systemic elevation in ROS, NO and TBARS levels, as well as MPO activity. Also, it upregulated the cellular activities of the enzymatic (SOD, and GPx) and non-enzymatic (TAC and GSH) antioxidants. Furthermore, the gene expression of the ROS-related necroinflammatory mediators (NF-κB, iNOS, COX-2, and TNF-α) in the kidney, brain, and spleen, as well as IL-1β, and IL-8 in the lung were greatly restored. The histopathological studies confirmed these biochemical results and showed a noticeable enhancing effect in the architecture of the studied organs after VVPF intake. Thus, this study indicated that VVPF had an alleviative effect on CCl4-induced necroinflammation and oxidative stress in rat kidney, lung, brain, and spleen via controlling the ROS/NF-κB pathway.

Induction of cyclooxygenase (COX)-2 but not COX-1 gene expression in apoptotic cell death

1998 ◽  
Vol 89 (1-2) ◽  
pp. 142-149 ◽  
Author(s):  
Lap Ho ◽  
Hiroshi Osaka ◽  
Paul S Aisen ◽  
Giulio Maria Pasinetti
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cox 2 ◽  
Cox 1

scholarly journals Oxytocin Promotes C6 Glial Cell Death and Aggravates Hydrogen Peroxide-induced Oxidative Stress

2020 ◽  
pp. 27-33
Author(s):  
Ahmet Sevki Taskiran ◽  
Merve Ergul
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Cell Viability ◽  
Glial Cell ◽  
Glial Cells ◽  
Control Group ◽  
C6 Cells ◽  
Cox 2 ◽  
Cox 1

Background. Recent studies have shown that oxytocin plays a vital role in neurons and glial cells. However, its effect on hydrogen peroxide (H2O2)-induced oxidative stress as well as cyclooxygenase-1 (COX-1) and COX-2 in glial cells are still unclear. Objective. This study aims to examine the effect of oxytocin on glial cell viability, oxidative stress, COX-1, and COX-2 in C6 glial cells after exposure to H2O2. Methods. In this study, C6 glioma cell line was used to study the effect of oxytocin on the glial cell in four cell groups. The control group was untreated. Cells in the H2O2 group were treated with 0.5 mM H2O2 for 24 h. Cells in the oxytocin group were treated with various concentrations (0.25, 0.5, 1, and 2 μg/mL) of oxytocin for 24 h. Cells in the oxytocin+H2O2 group were pre-treated with various concentrations (0.25, 0.5, 1, and 2 μg/mL) of oxytocin for 1 h before 24-h exposure to 0.5 mM H2O2. Cell viability was evaluated using XTT assay. Total antioxidant status and total oxidant status (TOS), COX-1, and COX-2 levels in the cells were measured by commercial kits. Results. Oxytocin with various concentrations significantly decreased the viability of C6 cells after H2O2-induced oxidative stress (P < 0.01). It also significantly increased the levels of TOS, COX-1, and COX-2 in C6 cells after H2O2-induced oxidative stress (P < 0.001). Conclusion. Oxytocin increases glial cell death after H2O2-induced oxidative damage in C6 cells, along with upregulation of COX-1 and COX-2 levels.

scholarly journals Considering the Effect of Rosa damascena Mill. Essential Oil on Oxidative Stress and COX-2 Gene Expression in the Liver of Septic Rats

2019 ◽  
Vol 16 (4) ◽  
pp. 416-424 ◽  
Author(s):  
Abolfazl DADKHAH ◽  
Faezeh FATEMI ◽  
Mohammad Reza Mohammadi MALAYERI ◽  
Mohammad Hassan Karvin ASHTIYANI ◽  
Sakineh Kazemi NOUREINI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Essential Oil ◽  
Rosa Damascena ◽  
Cox 2 ◽  
I Gene
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