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Journal articles on the topic 'Cyclooxygenase (COX)'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Zhang, Xinping, Scott G. Morham, Robert Langenbach, and Donald A. Young. "Malignant Transformation and Antineoplastic Actions of Nonsteroidal Antiinflammatory Drugs (Nsaids) on Cyclooxygenase-Null Embryo Fibroblasts." Journal of Experimental Medicine 190, no. 4 (1999): 451–60. http://dx.doi.org/10.1084/jem.190.4.451.

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In this study, we use primary embryonic fibroblasts derived from cyclooxygenase-deficient transgenic embryos to further investigate the role of the two cyclooxygenases, cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2), in the process of neoplastic transformation. Cells with either, neither, or both of the cyclooxygenases were transformed by Ha-ras and/or SV40. Our results show that when a cyclooxygenase enzyme is present, the transformed cells have marked increases in COX-2 and/or COX-1 expression. Nevertheless, each type of cell, deficient in either or both cyclooxygenases, can be readil

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2

Rodler, D., and Fred Sinowatz. "Expression of Prostaglandin-Synthesizing Enzymes (Cyclooxygenase 1, Cyclooxygenase 2) in the Ovary of the Quail (Coturnix japonica)." Folia Biologica 61, no. 4 (2015): 125–33. http://dx.doi.org/10.14712/fb2015061040125.

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Cyclooxygenase is known to be the ratelimiting enzyme in the production of prostaglandins. So far, in different bird species there have been found two isoforms of cyclooxygenases (COX), cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2). These isoforms along with prostaglandins are regarded to possess a determining influence on the success in female reproduction. Only in a few bird species the expression sites of cyclooxygenases have been investigated. In this study we report on the expression of COX-1 and COX-2 in the ovary of the quail (Coturnix japonica) using PCR, immunohistochemistry a

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3

Kutil, Zsofia, Veronika Temml, David Maghradze, et al. "Impact of Wines and Wine Constituents on Cyclooxygenase-1, Cyclooxygenase-2, and 5-Lipoxygenase Catalytic Activity." Mediators of Inflammation 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/178931.

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Cyclooxygenases and lipoxygenases are proinflammatory enzymes; the former affects platelet aggregation, vasoconstriction, vasodilatation and later the development of atherosclerosis. Red wines from Georgia and central and western Europe inhibited cyclooxygenase-1 (COX-1) activity in the range of 63–94%, cyclooxygenase-2 (COX-2) activity in the range of 20–44% (tested at a concentration of 5 mL/L), and 5-lipoxygenase (5-LOX) activity in the range of 72–84% (at a concentration of 18.87 mL/L). White wines inhibited 5-LOX in the range of 41–68% at a concentration of 18.87 mL/L and did not inhibit

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4

Reitz, David B., and Peter C. Isakson. "Cyclooxygenase-2 Inhibitors." Current Pharmaceutical Design 1, no. 2 (1995): 211–20. http://dx.doi.org/10.2174/1381612801666220917221427.

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Prostaglandins are synthesized by the enzyme cyclooxygenase (COX), which is the target for nonsteroidal anti-inflammatory drugs (NSAIDs). Recently a second form of COX was discovered (COX-2) that is induced by inflammatory stimuli. The identification of an inducible form of COX led to the hypothesis that COX-2 is responsible for inflammatory prostaglandins, whereas the constitutive COX-I produces physiologically important prostaglandins, e.g., in stomach and kidney. Selective COX- 2 inhibitors have been shown to be anti-inflammatory but do not cause ulcers in the stomach or intestines. It is a

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5

Chandrakirana Krisnamurti, Gabriella, and Fatchiyah Fatchiyah. "The Biological Function Prediction of The 10-gingerol Compound of Ginger in Inhibiting Cyclooxygenase-2 Activity." Journal of Pure and Applied Chemistry Research 9, no. 3 (2020): 222–32. http://dx.doi.org/10.21776/ub.jpacr.2020.009.03.547.

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Anti-inflammatory agents inhibit prostaglandin synthesis by blocking cyclooxygenases (COXs). The compounds extracted from ginger, 10-gingerol and 10-shogaol can inhibit inflammation but the mechanism of inhibition remains unclear. Here we used molecular docking to predict the molecular interactions between COXs and the three inhibitors, acetaminophen (CID1983), 10-gingerol (CID168115) and 10-shogaol (CID6442612). By using that acetaminophen as a gold standard, the results demonstrated that acetaminophen, 10-gingerol, and 10-shogaol could bind catalytic domain and membrane binding domain of cyc

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6

Belton, Orina, and Desmond J. Fitzgerald. "Cyclooxygenase isoforms and atherosclerosis." Expert Reviews in Molecular Medicine 5, no. 9 (2003): 1–18. http://dx.doi.org/10.1017/s1462399403005842.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of arthritis and pain. However, their long-term use is limited by gastrointestinal (GI) side effects such as gastric ulcers. NSAIDs act by inhibiting an enzyme called cyclooxygenase. Cyclooxygenase (COX) catalyses the generation of prostaglandins from arachidonic acid. Two isoforms of the enzyme exist – COX-1 and COX-2 – both of which are targets for NSAIDs. Although they are associated with GI toxicity, NSAIDs have important antithrombotic and anti-inflammatory effects. The GI injury has been attributed to COX-1 in

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7

Brannon, Timothy S., Amy N. MacRitchie, Marina A. Jaramillo, et al. "Ontogeny of cyclooxygenase-1 and cyclooxygenase-2 gene expression in ovine lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 1 (1998): L66—L71. http://dx.doi.org/10.1152/ajplung.1998.274.1.l66.

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Prostacyclin is a key mediator of pulmonary vascular and parenchymal function during late fetal and early postnatal life, and its synthesis in whole lung increases during that period. The rate-limiting enzyme in prostacyclin synthesis in the developing lung is cyclooxygenase (COX). We investigated the ontogeny and cellular localization of COX-1 (constitutive) and COX-2 (inducible) gene expression in lungs from late-gestation fetal lambs, 1-wk-old newborn lambs (NB1), and 1- to 4-mo-old newborn lambs (NB2). COX-1 mRNA abundance rose progressively from fetal to NB1 to NB2, increasing 12-fold ove

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8

Odau, Simone, Christoph Gabler, Christoph Holder, and Ralf Einspanier. "Differential expression of cyclooxygenase 1 and cyclooxygenase 2 in the bovine oviduct." Journal of Endocrinology 191, no. 1 (2006): 263–74. http://dx.doi.org/10.1677/joe.1.06761.

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The aim of the present study was to investigate the enzymes for the local prostaglandin (PG) biosynthesis present in the bovine oviduct during the estrous cycle to influence early reproductive events. Bovine oviducts were classified into four phases: pre-ovulatory, post-ovulatory, early-to-mid luteal, and late luteal phase, subdivided further into ipsi- or contralateral site and separated into ampulla or isthmus. Oviductal cells were gained by flushing the oviductal regions. Quantitative real-time reverse transcriptase-PCR was performed for the secretory and cytosolic phospholipases A2 (sPLA2I

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Hofer, Michal, and Milan Pospíšil. "Stimulated recovery of perturbed haematopoiesis by inhibition of prostaglandin production — promising therapeutic strategy." Open Life Sciences 1, no. 4 (2006): 584–93. http://dx.doi.org/10.2478/s11535-006-0033-3.

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AbstractInhibitors of prostaglandin production, designated as classical non-steroidal anti-inflammatory drugs (NSAIDs) and acting on the base of non-selective inhibition of cyclooxygenases, have been found in numerous studies to potentiate recovery of perturbed haematopoiesis by removing the negative feedback control mediated by prostaglandins. However, classical NSAIDs show pronounced undesirable gastrointestinal side effects, which limits the possibility of their utilization for various pathophysiological states including myelosuppression. Specific cyclooxygenase-2 (COX-2) inhibitors, target

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Hayes, Maria, Rotimi E. Aluko, Elena Aurino, and Leticia Mora. "Generation of Bioactive Peptides from Porphyridium sp. and Assessment of Their Potential for Use in the Prevention of Hypertension, Inflammation and Pain." Marine Drugs 21, no. 8 (2023): 422. http://dx.doi.org/10.3390/md21080422.

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Inflammation, hypertension, and negative heart health outcomes including cardiovascular disease are closely linked but the mechanisms by which inflammation can cause high blood pressure are not yet fully elucidated. Cyclooxygenase (COX) enzymes play a role in pain, inflammation, and hypertension development, and inhibition of these enzymes is currently of great interest to researchers and pharmaceutical companies. Non-steroidal anti-inflammatory drugs are the drug of choice in terms of COX inhibition but can have negative side effects for consumers. Functional food ingredients containing cyclo

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Glomb, Teresa, Benita Wiatrak, Katarzyna Gębczak, et al. "New 1,3,4-Oxadiazole Derivatives of Pyridothiazine-1,1-Dioxide with Anti-Inflammatory Activity." International Journal of Molecular Sciences 21, no. 23 (2020): 9122. http://dx.doi.org/10.3390/ijms21239122.

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Numerous studies have confirmed the coexistence of oxidative stress and inflammatory processes. Long-term inflammation and oxidative stress may significantly affect the initiation of the neoplastic transformation process. Here, we describe the synthesis of a new series of Mannich base-type hybrid compounds containing an arylpiperazine residue, 1,3,4-oxadiazole ring, and pyridothiazine-1,1-dioxide core. The synthesis was carried out with the hope that the hybridization of different pharmacophoric molecules would result in a synergistic effect on their anti-inflammatory activity, especially the

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Ray, Neelanjana, Margaret E. Bisher, and L. W. Enquist. "Cyclooxygenase-1 and -2 Are Required for Production of Infectious Pseudorabies Virus." Journal of Virology 78, no. 23 (2004): 12964–74. http://dx.doi.org/10.1128/jvi.78.23.12964-12974.2004.

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ABSTRACT We have recently shown that cyclooxygenase-2 (COX-2) transcription is markedly induced after herpes simplex virus type 1 and pseudorabies virus (PRV) infections of rat embryonic fibroblast (REF) cells (N. Ray and L. W. Enquist, J. Virol. 78:3489-3501, 2004). For this study, we investigated the role of cyclooxygenase induction in the replication and growth of PRV. We demonstrate here a concordant increase in COX-2 mRNA and protein levels after the infection of REF cells. Inhibitors blocking the activity of cyclooxygenases caused a dramatic reduction in PRV growth. Viral growth could be

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13

Maloney, Christopher G., William A. Kutchera, Kurt H. Albertine, Thomas M. McIntyre, Stephen M. Prescott, and Guy A. Zimmerman. "Inflammatory Agonists Induce Cyclooxygenase Type 2 Expression by Human Neutrophils." Journal of Immunology 160, no. 3 (1998): 1402–10. http://dx.doi.org/10.4049/jimmunol.160.3.1402.

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Abstract The synthesis of prostanoids is regulated by cyclooxygenases (prostaglandin H synthases), which catalyze the conversion of arachidonic acid to PGH2. Cyclooxygenases are the target of aspirin and other nonsteroidal anti-inflammatory agents. In this study, we found that human polymorphonuclear leukocytes (PMNs) express the inducible isoform of cyclooxygenase, COX-2, when stimulated by LPS whereas the protein was not detectable in freshly isolated human PMNs. We also found by immunohistochemical analysis that COX-2 is expressed in PMNs in inflamed human tissues. COX-2 was induced in a ti

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14

Mengle-Gaw, Laurel J., and Benjamin D. Schwartz. "Cyclooxygenase-2 inhibitors: promise or peril?" Mediators of Inflammation 11, no. 5 (2002): 275–86. http://dx.doi.org/10.1080/09629350290000041.

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The discovery of two isoforms of the cyclooxygenase enzyme, COX-1 and COX-2, and the development of COX-2-specific inhibitors as anti-inflammatories and analgesics have offered great promise that the therapeutic benefits of NSAIDs could be optimized through inhibition of COX-2, while minimizing their adverse side effect profile associated with inhibition of COX-1. While COX-2 specific inhibitors have proven to be efficacious in a variety of inflammatory conditions, exposure of large numbers of patients to these drugs in postmarketing studies have uncovered potential safety concerns that raise

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15

Listyani, Tiara Ajeng, Muniroh Addawiyyah, Danang Raharjo, and Pang Jyh Chyang. "Docking and Structural Modification of Flavonoid Derivative Compounds as Cycloxygenas-2 Enzyme Inhibitors." Indonesian Journal of Global Health Research 7, no. 1 (2024): 311–22. http://dx.doi.org/10.37287/ijghr.v7i1.4041.

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Seven flavonoid compounds have the activity of inhibiting the cyclooxygenase-2 (COX-2) enzyme, thus providing an anti-inflammatory effect. Molecular docking analysis is needed to determine the binding interaction between flavonoid compounds and the cyclooxygenase-2 (COX-2) enzyme. Objective: This study aims to determine the interaction of flavonoid compounds with the cyclooxygenase-2 (COX-2) enzyme along with the modification of the flavonoid compound structure to increase the binding energy to the cyclooxygenase-2 (COX-2) enzyme. Method: Flavonoid derivative compounds were geometry optimized

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Krämer, Bernhard K., Martin C. Kammerl, and Martin Kömhoff. "Renal Cyclooxygenase-2 (Cox-2)." Kidney and Blood Pressure Research 27, no. 1 (2004): 43–62. http://dx.doi.org/10.1159/000075811.

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Gosepath, Jan, Juergen Brieger, and Wolf J. Mann. "New Immunohistologic Findings on the Differential Role of Cyclooxygenase 1 and Cyclooxygenase 2 in Nasal Polyposis." American Journal of Rhinology 19, no. 2 (2005): 111–17. http://dx.doi.org/10.1177/194589240501900201.

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Background Cyclooxygenase 1 (Cox-1) plays a key role in arachidonic acid metabolism and in the pathophysiology and immunology of nasal polyposis in patients suffering from aspirin intolerance. We hypothesize that Cox-2 also might be relevant in the etiology of nasal polyps of aspirin-tolerant patients by their effects on inflammatory mediators as well as on microvascular permeability. Methods Fifty-two surgical specimens were immunohistochemically labeled for Cox-1 and Cox-2. Specimens were taken from chronically inflamed mucosa (n = 19) and from nasal polyps (n = 19) during endonasal sinus su

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Vernieri, Ermelinda, Isabel Gomez-Monterrey, Ciro Milite, et al. "Design, Synthesis, and Evaluation of New Tripeptides as COX-2 Inhibitors." Journal of Amino Acids 2013 (February 26, 2013): 1–7. http://dx.doi.org/10.1155/2013/606282.

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Cyclooxygenase (COX) is a key enzyme in the biosynthetic pathway leading to the formation of prostaglandins, which are mediators of inflammation. It exists mainly in two isoforms COX-1 and COX-2. The conventional nonsteroidal anti-inflammatory drugs (NSAIDs) have gastrointestinal side effects because they inhibit both isoforms. Recent data demonstrate that the overexpression of these enzymes, and in particular of cyclooxygenases-2, promotes multiple events involved in tumorigenesis; in addition, numerous studies show that the inhibition of cyclooxygenases-2 can delay or prevent certain forms o

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Mandic, Aljosa, Slavica Usaj-Knezevic, Tatjana Ivkovic-Kapicl, Dejan Nincic, and Goran Malenkovic. "Cyclooxygenase-2 expression in cervical cancer." Vojnosanitetski pregled 71, no. 11 (2014): 997–1005. http://dx.doi.org/10.2298/vsp1411997m.

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Background/Aim. Cyclooxygenase (COX) or prostaglandin H2 synthase is the first enzyme that catalyzes the first two steps in the biosynthesis of prostaglandins from arachidonic acid. The aim of the study was to determine the expression level of COX-2 in patients with cervical cancer and compare it with that in the control group with no cervical pathology. Methods. The study included 76 patients divided into two groups: the control group - 30 patients without histopathological changes and the group A - 46 patients with cervical cancer, FIGO stage IB-IIA. Histopathological and immunohistochemical

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Dickens, David S., Rafal Kozielski, Javed Khan, Anne Forus, and Timothy P. Cripe. "Cyclooxygenase-2 Expression in Pediatric Sarcomas." Pediatric and Developmental Pathology 5, no. 4 (2002): 356–64. http://dx.doi.org/10.1007/s10024-002-0005-1.

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Therapies for metastatic pediatric sarcomas have reached maximum tolerated doses, but continue to provide suboptimal cure rates. Additionally, these treatments are associated with numerous short- and long-term side effects. Therefore, the search for newer, less toxic therapeutic agents is warranted. Overexpression of the inducible enzyme, cyclooxygenase-2 (COX-2), has been discovered in a variety of adult solid tumors and numerous studies have shown COX-2 inhibitors to have significant antiproliferative effects. Therefore, we sought to determine the expression of COX-2 in pediatric sarcomas. W

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Thamm, D. H., E. J. Ehrhart, J. B. Charles, and Y. A. Elce. "Cyclooxygenase-2 Expression in Equine Tumors." Veterinary Pathology 45, no. 6 (2008): 825–28. http://dx.doi.org/10.1354/vp.45-6-825.

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The enzyme cyclooxygenase-2 (COX-2) is expressed in some tumor and stromal tissues, and catalyzes production of prostaglandins with growth stimulatory, antiapoptotic, proangiogenic, and immunosuppressive properties. Pharmacologic inhibition of COX-2 is associated with antitumor activity in various human and canine malignancies. The purpose of this study was to assess COX-2 expression in a series of equine sarcoids, melanomas, and squamous-cell carcinomas (SCC). COX-2 expression was assessed in formalin-fixed paraffin-embedded tissues from 14 sarcoids, 11 melanomas, and 37 SCC that represent va

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Prasojo, Stefanus Layli, Fajar Agung Dwi Hartanto, Nunung Yuniarti, Zullies Ikawati, and Enade Perdana Istyastono. "DOCKING OF 1-PHENYLSULFONAMIDE-3-TRIFLUOROMETHYL-5-PARABROMOPHENYL-PYRAZOLE TO CYCLOOXYGENASE-2 USING PLANTS." Indonesian Journal of Chemistry 10, no. 3 (2010): 348–51. http://dx.doi.org/10.22146/ijc.21441.

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The docking protocols to virtually screen selective cyclooxygenase-2 (COX-2) ligands using PLANTS docking software were developed and validated. The crystal structure of 1-phenylsulfonamide-3-trifluoromethyl-5-parabromophenyl-pyrazole (S58) binds to cyclooxygenase-2 (COX-2) was used as the reference structure. The developed protocols could predict the binding pose of S58 to COX-2 accurately (RMSD is 1.2 Ǻ).

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Harris, Raymond C., and Ming‐Zhi Zhang. "Cyclooxygenase Metabolites in the Kidney." Comprehensive Physiology 1, no. 4 (2011): 1729–58. https://doi.org/10.1002/j.2040-4603.2011.tb00382.x.

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AbstractIn the mammalian kidney, prostaglandins (PGs) are important mediators of physiologic processes, including modulation of vascular tone and salt and water. PGs arise from enzymatic metabolism of free arachidonic acid (AA), which is cleaved from membrane phospholipids by phospholipase A2 activity. The cyclooxygenase (COX) enzyme system is a major pathway for metabolism of AA in the kidney. COX are the enzymes responsible for the initial conversion of AA to PGG2 and subsequently to PGH2, which serves as the precursor for subsequent metabolism by PG and thromboxane synthases. In addition to

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Loy, A. H. C., T. C. Putti, and L. K. S. Tan. "Cyclooxygenase-2 expression in Warthin's tumour." Journal of Laryngology & Otology 119, no. 7 (2005): 515–18. http://dx.doi.org/10.1258/0022215054352117.

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Objectives: To determine whether cyclooxygenase-2 (COX-2) is overexpressed in Warthin's tumours, and to characterize its pattern of expression.Methods: Twenty-one paraffin-embedded Warthin's tumour specimens were analysed by immunohistochemical staining for expression of human COX-2. Semi-quantitative analysis of the staining was performed.Results: In all of the specimens, we found that there was overexpression of COX-2 within the epithelial component of the tumours, with no expression in the lymphoid components. There was also overexpression of COX-2 in the salivary duct system of normal paro

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Chillingworth, Naomi L., Scott G. Morham, and Lucy F. Donaldson. "Sex differences in inflammation and inflammatory pain in cyclooxygenase-deficient mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 2 (2006): R327—R334. http://dx.doi.org/10.1152/ajpregu.00901.2005.

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There are two cyclooxygenase (COX) genes encoding characterized enzymes, COX-1 and COX-2. Nonsteroidal anti-inflammatory drugs are commonly used as analgesics in inflammatory arthritis, and these often inhibit both cyclooxygenases. Recently, inhibitors of COX-2 have been used in the treatment of inflammatory arthritis, as this isoform is thought to be critical in inflammation and pain. The objective of this study was to determine the effect of COX-1 or COX-2 gene disruption on the development of chronic Freund’s adjuvant-induced arthritis and inflammatory pain in male and female mice. The effe

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Szweda, Marta, Andrzej Rychlik, Izabella Babińska, and Andrzej Pomianowski. "Significance of cyclooxygenase-2 in oncogenesis." Journal of Veterinary Research 63, no. 2 (2019): 215–24. http://dx.doi.org/10.2478/jvetres-2019-0030.

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Abstract The cyclooxygenase-2 (COX-2) enzyme catalyses the first stage of biosynthesis of prostanoids, proteins that are implicated in various physiological and pathological processes in humans and animals. The expression of COX-2 increases significantly during pathological processes accompanied by inflammation, pain and fever. Overexpression of COX-2 was determined in tumour tissues, which suggests that this enzyme participates in oncogenesis. In this paper the topics discussed are mechanisms regulating COX-2 expression, COX isoforms, their role in the body and the oncogenic mechanisms trigge

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Iñiguez, Miguel A., Carmen Punzón, and Manuel Fresno. "Induction of Cyclooxygenase-2 on Activated T Lymphocytes: Regulation of T Cell Activation by Cyclooxygenase-2 Inhibitors." Journal of Immunology 163, no. 1 (1999): 111–19. http://dx.doi.org/10.4049/jimmunol.163.1.111.

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Abstract Cyclooxygenase (COX), known to exist in two isoforms, COX-1 and COX-2, is a key enzyme in prostaglandin synthesis and the target for most nonsteroidal anti-inflammatory drugs. In this study, we show that human T lymphocytes express the COX-2 isoenzyme. COX-2 mRNA and protein were induced in both Jurkat and purified T cells stimulated by TCR/CD3 or PMA activation. COX-2 mRNA was induced very early after activation and superinduced by protein synthesis inhibitors, whereas it was inhibited by the immunosuppressive drug cyclosporin A, identifying it as an early T cell activation gene. Int

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Bauer, A. K., L. D. Dwyer-Nield, and A. M. Malkinson. "High cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2) contents in mouse lung tumors." Carcinogenesis 21, no. 4 (2000): 543–50. http://dx.doi.org/10.1093/carcin/21.4.543.

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Krzyżak, Edward, Dominika Szkatuła, Benita Wiatrak, Tomasz Gębarowski, and Aleksandra Marciniak. "Synthesis, Cyclooxygenases Inhibition Activities and Interactions with BSA of N-substituted 1H-pyrrolo[3,4-c]pyridine-1,3(2H)-diones Derivatives." Molecules 25, no. 12 (2020): 2934. http://dx.doi.org/10.3390/molecules25122934.

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Inhibition of cyclooxygenase is the way of therapeutic activities for anti-inflammatory pharmaceuticals. Serum albumins are the major soluble protein able to bind and transport a variety of exogenous and endogenous ligands, including hydrophobic pharmaceuticals. In this study, a novel N-substituted 1H-pyrrolo[3–c]pyridine-1,3(2H)-diones derivatives were synthesized and biologically evaluated for their inhibitory activity against cyclooxygenases and interactions with BSA. In vitro, COX-1 and COX-2 inhibition assays were performed. Interaction with BSA was studied by fluorescence spectroscopy an

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Doré, M., I. Lanthier, and J. Sirois. "Cyclooxygenase-2 Expression in Canine Mammary Tumors." Veterinary Pathology 40, no. 2 (2003): 207–12. http://dx.doi.org/10.1354/vp.40-2-207.

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Mammary tumors are the most common neoplasms in female dogs. Induction of cyclooxygenase-2 (COX-2) has been implicated in various cancers in humans. However, expression of COX-2 has not been investigated in canine mammary tumors. Normal mammary gland ( n = 4), simple or complex adenomas ( n = 63), and simple or complex adenocarcinomas ( n = 84) were studied by immunohistochemistry. Results showed that COX-2 was not expressed in the normal gland but was detected in 24% of adenomas and in 56% of adenocarcinomas ( P < 0.001). The incidence of COX-2 expression and the intensity of the COX-2 sig

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Tong, Xin, Lei Yin, Shree Joshi, Daniel W. Rosenberg, and Charles Giardina. "Cyclooxygenase-2 Regulation in Colon Cancer Cells." Journal of Biological Chemistry 280, no. 16 (2005): 15503–9. http://dx.doi.org/10.1074/jbc.m411978200.

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We are interested in the mechanism of cyclooxygenase-2 (Cox-2) regulation in colon cancer cells because this knowledge could provide insight into colon carcinogenesis and suggest ways to suppress Cox-2 expression in colon tumors. Studying the HT-29 colon cancer cell line as a model, we found that Cox-2 mRNA and protein levels were activated over 10-fold by the inflammatory cytokine tumor necrosis factor (TNF)-α. Moreover, we found that the histone deacetylase inhibitors butyrate and trichostatin A could block Cox-2 activation in a gene-specific manner. TNF-α and butyrate did not significantly

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Kis, Bela, James A. Snipes, Toyohi Isse, Krisztina Nagy, and David W. Busija. "Putative Cyclooxygenase-3 Expression in Rat Brain Cells." Journal of Cerebral Blood Flow & Metabolism 23, no. 11 (2003): 1287–92. http://dx.doi.org/10.1097/01.wcb.0000090681.07515.81.

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Cyclooxygenase-3 (COX-3), a new acetaminophen-sensitive isoform of the COX family, has recently been cloned from canine tissues. Canine COX-3 apparently is identical to the full-length form of COX-1, with the exception that the COX-3 mRNA retains intron 1. Additionally, COX-3 mRNA expression is high in the brain. We investigated the expression of the putative rat COX-3 mRNA in primary cultures of neurons, astrocytes, endothelial cells, pericytes, and choroidal epithelial cells from the rat brain. Specific RT-PCR primers were designed to detect putative rat COX-3 mRNA, and the RT-PCR products w

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Zhang, Ming-Zhi, Jun-Ling Wang, H. F. Cheng, Raymond C. Harris, and James A. McKanna. "Cyclooxygenase-2 in rat nephron development." American Journal of Physiology-Renal Physiology 273, no. 6 (1997): F994—F1002. http://dx.doi.org/10.1152/ajprenal.1997.273.6.f994.

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The inducible second isoform of cyclooxygenase (COX-2) that mediates inflammation also is expressed at low levels in normal adult rat kidneys and is upregulated in response to noninflammatory stimuli (R. C. Harris, J. A. McKanna, Y. Akai, H. R. Jacobson, R. N. DuBois, and M. D. Breyer. J. Clin. Invest. 94: 2504–2510, 1994). Roles in morphogenesis are indicated by reported teratogenicity of COX inhibitors and renal dysgenesis in COX-2 knockout mice (J. E. Dinchuk, B. D. Car, R. J. Focht, J. J. Johnston, B. D. Jaffee, M. B. Covington, N. R. Contel, V. M. Eng, R. J. Collins, P. M. Czerniak, A. G.

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Reese, Jeff, Xuemei Zhao, Wen-Ge Ma, Naoko Brown, Timothy J. Maziasz, and S. K. Dey. "Comparative Analysis of Pharmacologic and/or Genetic Disruption of Cyclooxygenase-1 and Cyclooxygenase-2 Function in Female Reproduction in Mice*." Endocrinology 142, no. 7 (2001): 3198–206. http://dx.doi.org/10.1210/endo.142.7.8307.

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Abstract Cyclooxygenase (COX)-derived prostaglandins are critical in female reproduction. Gene targeting studies show that ovulation, fertilization, implantation, and decidualization are defective in COX-2 deficient mice. We used genetic and pharmacologic approaches to perturb COX function and examine the differential and synergistic effects of inhibition of COX-1, COX-2, or of both isoforms on reproductive outcomes during early pregnancy in mice. The results demonstrate that simultaneous inhibition of COX-1 and COX-2 produces more severe effects on early pregnancy events than inhibition of ei

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Schmassmann, Adrian, Georg Zoidl, Brigitta M. Peskar, et al. "Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 4 (2006): G747—G756. http://dx.doi.org/10.1152/ajpgi.00416.2005.

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Traditional NSAIDs, selective cyclooxygenase (COX)-2 inhibitors, and inhibitors of nitric oxide synthase (NOS) impair the healing of preexisting gastric ulcers. However, the role of COX-1 (with or without impairment of COX-2) and the interaction between COX and NOS isoforms during healing are less clear. Thus we investigated healing and regulation of COX and NOS isoforms during ulcer healing in COX-1 and COX-2 deficiency and inhibition mouse models. In this study, female wild-type COX-1−/− and COX-2−/− mice with gastric ulcers induced by cryoprobe were treated intragastrically with vehicle, se

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Dewi, Tanaya Jati Dharma. "In Silico Study of Novel Ketorolac as selective Cyclooxygenase-2 (COX-2)." Proceeding Annual Symposium on Hajj and Umrah Medicine 1 (December 5, 2022): 93. https://doi.org/10.18860/anshar.v1i0.2138.

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Ketorolac is a non-selective non-steroidal anti-inflammatory drug (NSAID). Ketorolac works by inhibiting the enzymes Cyclooxygenase-1 (COX-1) and Cyclooxygenase-2(COX-2). Because it also interacts with it, it gives several side effects, especially on digestion. This study aimed to design and obtain a novel ketorolac, a modification of the ketorolac compound that is selective and does not interact with it. Modify the structure by adding a substituent at the para position in the benzene ring. The method was carried out in silico with molecular docking. Predictions were made from the physicochemi

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Ferreri, Nicholas R., Shao-Jian An, and John C. McGiff. "Cyclooxygenase-2 expression and function in the medullary thick ascending limb." American Journal of Physiology-Renal Physiology 277, no. 3 (1999): F360—F368. http://dx.doi.org/10.1152/ajprenal.1999.277.3.f360.

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The medullary thick ascending limb (MTAL) metabolizes arachidonic acid (AA) via cytochrome P-450 (CyP450)- and cyclooxygenase (COX)-dependent pathways. In the present study, we demonstrated that the COX-2-selective inhibitor, NS-398, prevented tumor necrosis factor-α (TNF)- and phorbol myristate acetate (PMA)-mediated increases in PGE2 production by cultured MTAL cells. Accumulation of COX-2, but not COX-1, mRNA increased when cells were challenged with TNF (1 nM) or PMA (1 μM). Pretreatment of cells for 30 min with actinomycin D (AcD, 1 μM) had little effect on COX-2 mRNA accumulation in unst

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Bronger, H., S. Kraeft, A. Stöckel, et al. "Effect of cyclooxygenase inhibition on CXCR3 ligand secretion in breast cancer." Journal of Clinical Oncology 29, no. 27_suppl (2011): 45. http://dx.doi.org/10.1200/jco.2011.29.27_suppl.45.

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45 Background: In murine cancer models, the two IFN-γ inducible chemokines CXCL9 and CXCL10, those bind to the common receptor CXCR3, recruit NK cells and tumor-suppressive lymphocytes into the tumor site and impair tumor growth and metastatic spread. In human breast cancer (BC), we and others have shown that high levels of CXCL9 mRNA correlate with favorable prognosis and the number of infiltrating lymphocytes. Raising the intratumoral level of CXCR3 ligands might therefore be a feasible way to enhance the infiltration by tumor-suppressive immune cells and to improve immune intervention in br

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Rassnick, Kenneth M., and Bradley L. Njaa. "Cyclooxygenase-2 Immunoreactivity in Equine Ocular Squamous-Cell Carcinoma." Journal of Veterinary Diagnostic Investigation 19, no. 4 (2007): 436–39. http://dx.doi.org/10.1177/104063870701900419.

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Squamous-cell carcinoma (SCC) is the second most common tumor in horses, and 40%-50% may occur in ocular and adnexal structures. Cyclooxygenase (COX)-2 is an inducible enzyme responsible for the production of prostaglandins that control cell growth and the development and progression of cancer. Mechanisms responsible for the initial upregulation of COX-2 in neoplasia are unclear; prolonged sunlight exposure and mutations in the p53 gene may be possibilities. Because the etiopathogenesis of ocular SCC in horses may involve ultraviolet sunlight and p53 mutations, the purpose of this study was to

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Rand, Amy A., Bogdan Barnych, Christophe Morisseau, et al. "Cyclooxygenase-derived proangiogenic metabolites of epoxyeicosatrienoic acids." Proceedings of the National Academy of Sciences 114, no. 17 (2017): 4370–75. http://dx.doi.org/10.1073/pnas.1616893114.

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Arachidonic acid (ARA) is metabolized by cyclooxygenase (COX) and cytochrome P450 to produce proangiogenic metabolites. Specifically, epoxyeicosatrienoic acids (EETs) produced from the P450 pathway are angiogenic, inducing cancer tumor growth. A previous study showed that inhibiting soluble epoxide hydrolase (sEH) increased EET concentration and mildly promoted tumor growth. However, inhibiting both sEH and COX led to a dramatic decrease in tumor growth, suggesting that the contribution of EETs to angiogenesis and subsequent tumor growth may be attributed to downstream metabolites formed by CO

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Abdelwahab, Siddig Ibrahim, Mohammed Al-Mamary, Khaled Hassanein, Manal Mohamed Elhassan Taha, Abdullah Farasani, and Hassan Alhazmi. "Effects of anti-cyclooxygenases (COX-1 and COX-2), structure activity relationship, molecular docking and in silico ADMET of some synthesized chalcones." Tropical Journal of Pharmaceutical Research 21, no. 11 (2023): 2419–27. http://dx.doi.org/10.4314/tjpr.v21i11.22.

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Purpose: To develop effective cancer chemopreventive and anti-inflammatory agents, a series of chalcones were prepared by reacting suitable aromatic aldehyde with appropriate acetophenones. Methods: Twenty-four synthesized chalcones (namely, 1 - 24) were assessed for their in vitro anti-cyclooxygenase-1 (COX-1) and anti-cyclooxygenase-2 (COX-2) activity in a COX catalyzed prostaglandin synthesis bioassay. Molecular docking was done to investigate the ligand-protein interactions, and selectivity on both enzymes. ADMET (absorption, distribution, metabolism, excretion, toxicity) modeling an

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Rachmania, Rizky Arcinthya, Hariyanti Hariyanti, Ririh Zikriah, and Aditya Sultan. "Studi In Silico Senyawa Alkaloid Herba Bakung Putih (Crinum Asiaticum L.) pada Penghambatan Enzim Siklooksigenase (COX)." Jurnal Kimia VALENSI 4, no. 2 (2018): 124–36. http://dx.doi.org/10.15408/jkv.v4i2.7686.

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Inflammation is a response to tissue injury involving the physiological process of cyclooxygenase enzyme activation which has two isoforms, cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes. The use of anti-inflammatory drugs of Non Steroidal Anti Inflammatory (AINS) and steroid groups has side effects in long-term use. The objective of this study was to find out eight active white herbic alkaloid compounds (Crinum asiaticum L.) to be used as anti-inflammatory by inhibiting COX-1 and COX-2 enzymes. Molecular docking method for the prediction of complex structures of proteins called

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Legan, Mateja, Boštjan Luzar, Vera Ferlan-Marolt, and Andrej Cör. "Cyclooxygenase-2 Expression Determines Neoangiogenesis in Gallbladder Carcinomas." Bosnian Journal of Basic Medical Sciences 6, no. 4 (2006): 58–63. http://dx.doi.org/10.17305/bjbms.2006.3122.

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Neo-angiogenesis may have an important role in the poor prognosis of gallbladder carcinoma. An enhanced expression of COX-2 was found in precancerous lesions and in gallbladder carcinoma, likely to be involved in carcinogenesis as well as in angiogenesis. To study the relationships between the COX-2 expression and degree of vascularization, as well as to evaluate their role in the prognosis of patients with gallbladder carcinoma. 27 cases of gallbladder adenocarcinoma were included, classified grading I-III according the WHO classification. The COX-2 and endothelial antigen CD105 expressions w

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Rubin, Bernard R. "Specific cyclooxygenase-2 (COX-2) inhibitors." Journal of the American Osteopathic Association 99, no. 6 (1999): 322. http://dx.doi.org/10.7556/jaoa.1999.99.6.322.

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Little, Dianne, Samuel L. Jones, and Anthony T. Blikslager. "Cyclooxygenase (COX) Inhibitors and the Intestine." Journal of Veterinary Internal Medicine 21, no. 3 (2007): 367–77. http://dx.doi.org/10.1111/j.1939-1676.2007.tb02978.x.

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46

Reuss-Borst, M. "Selektive Cyclooxygenase-2 (COX-2)-Hemmer." Der Internist 38, no. 3 (1997): 266–71. http://dx.doi.org/10.1007/s001080050040.

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Harris, Raymond C., and Matthew D. Breyer. "Physiological regulation of cyclooxygenase-2 in the kidney." American Journal of Physiology-Renal Physiology 281, no. 1 (2001): F1—F11. http://dx.doi.org/10.1152/ajprenal.2001.281.1.f1.

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In adult mammalian kidney, cyclooxygenase-2 (COX-2) expression is found in a restricted subpopulation of cells. The two sites of renal COX-2 localization detected in all species to date are the macula densa (MD) and associated cortical thick ascending limb (cTALH) and medullary interstitial cells (MICs). Physiological regulation of COX-2 in these cellular compartments suggests functional roles for eicosanoid products of the enzyme. COX-2 expression increases in high-renin states (salt restriction, angiotensin-converting enzyme inhibition, renovascular hypertension), and selective COX-2 inhibit

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48

Chida, M., and N. F. Voelkel. "Effects of acute and chronic hypoxia on rat lung cyclooxygenase." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 5 (1996): L872—L878. http://dx.doi.org/10.1152/ajplung.1996.270.5.l872.

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Cyclooxygenase-2 (COX-2) is an inducible cyclooxygenase enzyme and may play an important role in the pathogenesis of lung injury and in pulmonary vascular remodeling. In this study we determined the effects of acute or chronic hypoxia on COX-2 induction and its modulation by .NO and adenosine 3'-5'-cyclic monophosphate (cAMP). Isolated perfused rat lungs were exposed to a normoxic gas mixture or a hypoxic gas mixture for 3 h. Northern blot analysis showed that 3 h of acute hypoxia were sufficient to increase COX-2 but not COX-1 transcripts in the lung. COX-2 expression induced by acute hypoxia

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Saadi, Esraa, Rapita Sood, Ido Dromi, et al. "Limited Proteolysis of Cyclooxygenase-2 Enhances Cell Proliferation." International Journal of Molecular Sciences 21, no. 9 (2020): 3195. http://dx.doi.org/10.3390/ijms21093195.

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Accumulating evidence suggests that the cyclooxygenase-2 (COX-2) enzyme has additional catalytic-independent functions. Here we show that COX-2 appears to be cleaved in mouse and human tumors, which led us to hypothesize that COX-2 proteolysis may play a role in cell proliferation. The data presented herein show that a K598R point mutation at the carboxyl-terminus of COX-2 causes the appearance of several COX-2 immunoreactive fragments in nuclear compartments, and significantly enhances cell proliferation. In contrast, insertion of additional mutations at the border of the membrane-binding and

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A. Abdul Razzak, Nadeem, Samera F.Hussan, and Ahlam J. Qaseer. "Design and Synthesis of New Non-Steroidal Anti-inflammatory Agents with Expected Selectivity toward Cyclooxygenase-2 Inhibition." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 19, no. 1 (2017): 6–13. http://dx.doi.org/10.31351/vol19iss1pp6-13.

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This study includes design and synthesis of new non-steroidal anti-inflammatory agents (NSAIDs) with expected cyclooxygenase-2 (COX-2) selective inhibition to achieve better activity and low gastric side effects. Two series of compounds have been designed and synthesized as potential NSAIDs,these are: Salicylamide derivatives (compounds 3,4,5 ) and Diflunisal derivatives (compounds 10&11). In vivo acute anti-inflammatory effect of one of the synthesized agents (compound 3) was evaluated in the rat using egg-white induced paw edema model of inflammation. Preliminary pharmacological study re

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