Evaluation of the Effect of α-L-Guluronic Acid (G2013) on COX-1, COX-2 Activity and Gene Expression for Introducing this Drug as a Novel NSAID with Immunomodulatory Property

2018 ◽  
Vol 12 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Abbas Mirshafiey ◽  
Seyed S. Mortazavi-Jahromi ◽  
Mahsa Taeb ◽  
Salvatore Cuzzocrea ◽  
Emanuela Esposito
Keyword(s):  
Gene Expression ◽  
Immunomodulatory Property ◽  
Guluronic Acid ◽  
Cox 2 ◽  
Cox 1

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.

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

NO regulates LPS-stimulated cyclooxygenase gene expression and activity in pulmonary artery endothelium

2001 ◽  
Vol 280 (3) ◽  
pp. L450-L457 ◽  
Author(s):  
Jian-Xiong Chen ◽  
Leonard C. Berry ◽  
Brian W. Christman ◽  
Miles Tanner ◽  
Paul R. Myers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pulmonary Artery ◽  
Protein Expression ◽  
Gas Chromatography Mass Spectrometry ◽  
No Donors ◽  
Gene And Protein Expression ◽  
Cox 2 ◽  
Spermine Nonoate ◽  
Cox 1 ◽  
Expression And Activity

We examined whether nitric oxide (NO) inhibits prostanoid synthesis through actions on cyclooxygenase (COX) gene expression and activity. Bovine pulmonary artery endothelial cells were pretreated for 30 min with the NO donors 1 mM S-nitroso- N-acetylpenicillamine (SNAP), 0.5 mM sodium nitroprusside (SNP), or 0.2 μM spermine NONOate; controls included cells pretreated with either 1 mM N-acetyl-d-penicillamine or the NO synthase (NOS) inhibitor 1 mM N G-nitro-l-arginine methyl ester with and without addition of lipopolysaccharide (LPS; 0.1 μg/ml) for 8 h. COX-1 and COX-2 gene and protein expression were examined by RT-PCR and Western analysis, respectively; prostanoid measurements were made by gas chromatography-mass spectrometry, and COX activity was studied after a 30-min incubation with 30 μM arachidonic acid. LPS induced COX-2 gene and protein expression and caused an increase in COX activity and an eightfold increase in 6-keto-PGF1αrelease. LPS-stimulated COX-2 gene expression was decreased by ∼50% by the NO donors. In contrast, LPS caused a significant reduction in COX-1 gene expression and treatment with NO donors had little effect. SNAP, SNP, and NONOate significantly suppressed LPS-stimulated COX activity and 6-keto-PGF1α release. Our data indicate that increased generation of NO attenuates LPS-stimulated COX-2 gene expression and activity, whereas inhibition of endogenous NOS has little effect.

scholarly journals The potential of acetylsalicylic acid and vitamin E in modulating inflammatory cascades in chickens under lipopolysaccharide-induced inflammation

2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Paweł Konieczka ◽  
Marcin Barszcz ◽  
Paweł Kowalczyk ◽  
Michał Szlis ◽  
Jan Jankowski
Keyword(s):  
Gene Expression ◽  
Oxygen Consumption ◽  
Vitamin E ◽  
Acetylsalicylic Acid ◽  
Mrna Expression ◽  
Poultry Production ◽  
Lps Challenge ◽  
Immune Tissues ◽  
Cox 2 ◽  
Cox 1

Abstract Distinct enzymes, including cyclooxygenase 1 and 2 (COX-1 and COX-2), lipoxygenase (LOXs), and cytochrome P450 monooxygenase (CYP450), produce different stress mediators and mediate inflammation in birds. Bioactive agents such as acetylsalicylic acid (ASA) and vitamin E (vE) may affect enzyme activities and could be used in poultry production to control the magnitude of acute phase inflammation. Here, we characterized COX, LOX, and CYP450 mRNA expression levels in chicken immune tissues in response to Escherichia coli lipopolysaccharide (LPS) challenge and investigated whether ASA and vE could alter gene expression. Additionally, for the first time in chickens, we evaluated oxygen consumption by platelet mitochondria as a biomarker of mitochondria function in response to ASA- and vE. LPS challenge compromised bird growth rates, but neither dietary ASA nor vE significantly ameliorated this effect; however, gradually increasing dietary vE levels were more effective than basal levels. ASA regulated arachidonic acid metabolism, providing an eicosanoid synthesis substrate, whereas gradually increasing vE levels evoked aspirin resistance during challenge. Gene expression in immune tissues was highly variable, indicating a complex regulatory network controlling inflammatory pathways. However, unlike COX-1, COX-2 and CYP450 exhibited increased mRNA expression in some cases, suggesting an initiation of novel anti-inflammatory and pro-resolving signals during challenge. Measuring oxygen consumption rate, we revealed that neither the ASA nor vE levels applied here exerted toxic effects on platelet mitochondria.

scholarly journals LC-MS/MS Confirms That COX-1 Drives Vascular Prostacyclin Whilst Gene Expression Pattern Reveals Non-Vascular Sites of COX-2 Expression

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e69524 ◽  
Author(s):  
Nicholas S. Kirkby ◽  
Anne K. Zaiss ◽  
Paula Urquhart ◽  
Jing Jiao ◽  
Philip J. Austin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Cox 2 ◽  
Cox 1

scholarly journals Flavocoxid Inhibits Phospholipase A2, Peroxidase Moieties of the Cyclooxygenases (COX), and 5-Lipoxygenase, Modifies COX-2 Gene Expression, and Acts as an Antioxidant

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Bruce P. Burnett ◽  
Alessandra Bitto ◽  
Domenica Altavilla ◽  
Francesco Squadrito ◽  
Robert M. Levy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Phospholipase A2 ◽  
Peritoneal Macrophages ◽  
Mechanisms Of Action ◽  
Enzyme Assays ◽  
Molecular Pathways ◽  
Oxygen Species ◽  
Cox 2 ◽  
Cox 1

The multiple mechanisms of action for flavocoxid relating to arachidonic acid (AA) formation and metabolism were studiedin vitro. Flavocoxid titrated into rat peritoneal macrophage cultures inhibited cellular phospholipase A2 (PLA2) (IC50= 60 μg/mL). Inin vitroenzyme assays, flavocoxid showed little anti-cyclooxygenase (CO) activity on COX-1/-2 enzymes, but inhibited the COX-1 (IC50= 12.3) and COX-2 (IC50= 11.3 μg/mL) peroxidase (PO) moieties as well as 5-lipoxygenase (5-LOX) (IC50= 110 μg/mL). No detectable 5-LOX inhibition was found for multiple traditional and COX-2 selective NSAIDs. Flavocoxid also exhibited strong and varied antioxidant capacitiesin vitroand decreased nitrite levels (IC50= 38 μg/mL) in rat peritoneal macrophages. Finally, in contrast to celecoxib and ibuprofen, which upregulated thecox-2 gene, flavocoxid strongly decreased expression. This work suggests that clinically favourable effects of flavocoxid for management of osteoarthritis (OA) are achieved by simultaneous modification of multiple molecular pathways relating to AA metabolism, oxidative induction of inflammation, and neutralization of reactive oxygen species (ROS).

scholarly journals Inhibition of COX-2 and NF-κB1 Gene Expression, NO Production, 5-LOX, and COX-1 and COX-2 Enzymes by Extracts and Constituents of Onopordum acanthium

Planta Medica ◽  
2015 ◽  
Vol 81 (14) ◽  
pp. 1270-1276 ◽  
Author(s):  
Ildikó Lajter ◽  
San-Po Pan ◽  
Stefanie Nikles ◽  
Sabine Ortmann ◽  
Andrea Vasas ◽  
...  
Keyword(s):  
Gene Expression ◽  
No Production ◽  
Onopordum Acanthium ◽  
Cox 2 ◽  
Cox 1

COX and PTGDS Gene Expression Levels in PGD2 Synthesis Pathway are Correlated with miR-520 in Patients with Vessel Restenosis

2020 ◽  
Vol 20 (9) ◽  
pp. 1514-1522 ◽  
Author(s):  
Shima Rezaee ◽  
Naser Kakavandi ◽  
Mohammad Shabani ◽  
Mohsen Khosravi ◽  
Seyed R. Hosseini-Fard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostaglandin Synthesis ◽  
Expression Levels ◽  
Stent Restenosis ◽  
Subendothelial Space ◽  
Elisa Technique ◽  
Cox 2 ◽  
Cox 1 ◽  
In Stent Restenosis ◽  
Gene Expression Levels

Background: The vessel restenosis is related to the inflammatory events in subendothelial space. It is proposed that the inflammatory agents affect the prostaglandin synthesis pathway. In this study, we investigated the COX-1, COX-2, PTGDS and miRNA-520a-5p expression levels and the serum 15-Deoxy-Δ12,14-PGJ2 metabolite values in patients with the stenosed and re-stenosed vessels. Furthermore, the associations between genes and miR-520 were evaluated in the monocyte transfection studies. Methods: The subjects (n=60) were included three groups; healthy subjects (control (stenosis < 5%), stent no restenosis (SNR, restenosis < 5%) and in-stent restenosis (ISR, restenosis > 70%)). The miRNA and gene expression levels were measured by RT-qPCR technique. 15-Deoxy-Δ12,14-PGJ2 values were measured by the ELISA technique. The miR-520 was transfected into myocytes using PEI polymer. Results: The monocyte COX-1, COX-2 and PTGDS gene expression levels and the serum 15-Deoxy- Δ12,14-PGJ2 values increased significantly in the patients. Furthermore, the miR-520 correlated conversely with the COX-1, and PTGDS gene expression levels. Conclusion: The results showed that the PGD2 synthesis pathway is active in the patients and, miR- 520 may be involved in the function of this pathway.

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