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Pesquisa : D08.811.600.720 [Categoria DeCS]
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[PMID]:29235601
[Au] Autor:Mandal P; Kundu BK; Vyas K; Sabu V; Helen A; Dhankhar SS; Nagaraja CM; Bhattacherjee D; Bhabak KP; Mukhopadhyay S
[Ad] Endereço:Department of Chemistry, School of Basic Sciences, Indian Institute of Technology Indore, Indore 453552, India. suman@iiti.ac.in.
[Ti] Título:Ruthenium(ii) arene NSAID complexes: inhibition of cyclooxygenase and antiproliferative activity against cancer cell lines.
[So] Source:Dalton Trans;47(2):517-527, 2018 Jan 02.
[Is] ISSN:1477-9234
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Non-steroidal anti-inflammatory drugs (NSAIDs) are a group of molecules which have been found to be active against cancer cells with chemopreventive properties by targeting cyclooxygenase (COX-1 and COX-2) and lipoxygenase (LOX), commonly upregulated (particularly COX-2) in malignant tumors. Arene ruthenium(ii) complexes with a pseudo-octahedral coordination environment containing different ancillary ligands have shown remarkable activity against primary and metastatic tumors as reported earlier. This work describes the synthesis of four novel ruthenium(ii)-arene complexes viz. [Ru(η -p-cymene)(nap)Cl] 1 [Hnap = naproxen or (S)-2-(6-methoxy-2-naphthyl)propionic acid], [Ru(η -p-cymene)(diclo)Cl] 2 [Hdiclo = diclofenac or 2-[(2,6-dichlorophenyl)amino] benzeneacetic acid, [Ru(η -p-cymene)(ibu)Cl] 3 [Hibu = ibuprofen or 2-(4-isobutylphenyl)propanoic acid] and [Ru(η -p-cymene)(asp)Cl] 4 [Hasp = aspirin or 2-acetoxy benzoic acid] using different NSAIDs as chelating ligands. Complexes 1-3 have shown promising antiproliferative activity against three different cell lines with GI (concentration of drug causing 50% inhibition of cell growth) values comparable to adriamycin. At the concentration of 50 µM, complex 3 is more effective in the inhibition of cyclooxygenase and lipooxygenase enzymes, followed by complex 2 and complex 1 in comparison to their respective free NSAID ligands indicating a possible correlation between the inhibition of COX and/or LOX and anticancer properties. Molecular docking studies with COX-2 reveal that complexes 1 and 2 having naproxen and diclofenac ligands exhibit stronger interactions with COX-2 than their respective free NSAIDs and these results are in good agreement with their relative experimentally observed COX inhibition as well as anti-proliferative activities.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/química
Benzeno/química
Compostos Organometálicos/química
Compostos Organometálicos/farmacologia
Prostaglandina-Endoperóxido Sintases/metabolismo
Rutênio/química
[Mh] Termos MeSH secundário: Animais
Bovinos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Ciclo-Oxigenase 1/química
Ciclo-Oxigenase 1/metabolismo
Ciclo-Oxigenase 2/química
Ciclo-Oxigenase 2/metabolismo
Inibidores de Ciclo-Oxigenase/síntese química
Inibidores de Ciclo-Oxigenase/química
Inibidores de Ciclo-Oxigenase/metabolismo
Inibidores de Ciclo-Oxigenase/farmacologia
DNA/metabolismo
Dimetil Sulfóxido/química
Estabilidade de Medicamentos
Seres Humanos
Lipoxigenase/metabolismo
Inibidores de Lipoxigenase/síntese química
Inibidores de Lipoxigenase/química
Inibidores de Lipoxigenase/metabolismo
Inibidores de Lipoxigenase/farmacologia
Simulação de Acoplamento Molecular
Compostos Organometálicos/síntese química
Compostos Organometálicos/metabolismo
Prostaglandina-Endoperóxido Sintases/química
Conformação Proteica
Soroalbumina Bovina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase Inhibitors); 0 (Lipoxygenase Inhibitors); 0 (Organometallic Compounds); 27432CM55Q (Serum Albumin, Bovine); 7UI0TKC3U5 (Ruthenium); 9007-49-2 (DNA); EC 1.13.11.12 (Lipoxygenase); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); J64922108F (Benzene); YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1039/c7dt03637j


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[PMID]:29173788
[Au] Autor:Aranda JV; Salomone F; Valencia GB; Beharry KD
[Ad] Endereço:State University of New York Downstate Medical Center, 450 Clarkson Avenue, Box 49, Brooklyn, NY 11203, USA. Electronic address: jacob.aranda@downstate.edu.
[Ti] Título:Non-steroidal Anti-inflammatory Drugs in Newborns and Infants.
[So] Source:Pediatr Clin North Am;64(6):1327-1340, 2017 Dec.
[Is] ISSN:1557-8240
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nonsteroidal antiinflammatory drugs (NSAIDs) and acetaminophen are used in young infants and newborns for pain and fever control, patent ductus closure, prevention of intraventricular hemorrhage, and potentially for prevention of retinopathy of prematurity. These drugs inhibit cyclooxygenase 1 (COX-1), COX-2, and peroxidases, thus, blocking prostaglandin (PG) synthesis. PGs are eicosanoids that regulate several physiologic, pathologic, and cellular processes, including vasomotor tone, platelet aggregation, sensitization of neurons to pain, and many molecular events critical to physiologic homeostasis. NSAIDs inhibit caspases and cell death. Increasing knowledge of these molecular entities may allow targeted drug development to prevent or minimize neonatal morbidities.
[Mh] Termos MeSH primário: Acetaminofen/uso terapêutico
Analgésicos não Entorpecentes/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Prostaglandina-Endoperóxido Sintases/efeitos dos fármacos
[Mh] Termos MeSH secundário: Seres Humanos
Lactente
Recém-Nascido
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Anti-Inflammatory Agents, Non-Steroidal); 362O9ITL9D (Acetaminophen); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:27773348
[Au] Autor:Rebordão MR; Galvão A; Pinto-Bravo P; Pinheiro J; Gamboa S; Silva E; Mateus L; Ferreira-Dias G
[Ad] Endereço:CIISA, Faculty of Veterinary Medicine, University of Lisbon, Lisbon, Portugal; Department of Animal Science, Coimbra College of Agriculture, Coimbra, Portugal.
[Ti] Título:Endometrial prostaglandin synthases, ovarian steroids, and oxytocin receptors in mares with oxytocin-induced luteal maintenance.
[So] Source:Theriogenology;87:193-204, 2017 Jan 01.
[Is] ISSN:1879-3231
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxytocin (OXT) has been used to prolong the luteal phase in mares, but its mechanism of action is unknown. The aim of this study was to evaluate the effect of chronic exogenous OXT administration to mid-luteal phase mares on luteal maintenance. Also, endometrial expression of prostaglandin endoperoxide synthase 2 (PTGS2), prostaglandin F α, E and I synthases (AKR1C3, PTGES, and PTGIS), oxytocin receptor (OXTR), progesterone receptor (PGR), and estrogen receptors 1 (ESR1) and 2 (ESR2) were assessed in mares experiencing luteal maintenance 2 weeks after chronic exogenous OXT administration. Control mares (n = 5; C group) received 6 mL of saline im, whereas OXT (60 units/mare) was administered im (n = 6; OXT group), every 12 hours, on days 7 to 14 postovulation. After endometrial biopsy in groups C (Day 10) and OXT (Day 24), luteolysis occurred within 3 or 6 days, respectively. Luteal maintenance took place in 4 of 6 (67%) of OXT-treated mares. Progesterone in C group was the highest on biopsy day (P < 0.05). In OXT mares, PTGS2, ESR1 (P < 0.05), PTGES, PTGIS, PGR, and ESR2 (P < 0.01) gene transcription decreased, whereas OXTR increased (P < 0.05) in comparison with the C group. In OXT-treated mares, endometrial ESR2 protein expression decreased (P < 0.05), but OXTR increased (P < 0.05) compared with control animals. In both experimental groups, PTGS2 was mainly immunolocalized in surface epithelium, whereas AKR1C3, PTGES, PTGIS, and PGR were in surface and glandular epithelia. ESR1 and ESR2 were found in glandular epithelium and OXTR in stromal cells. High immunolabeling for PTGES, PTGIS, PGR, and OXTR and low for ESR2 was detected in endometrium of OXT-group mares with extended diestrus. Prolonged luteal function associated with chronic OXT treatment may be related to different spatial expression of OXTR and PGR in the endometrium. The observed reduction of endometrial ESR2 may be responsible for the maintenance of PGR in luminal and glandular epithelium. Also, ESR2 may attenuate the transcriptional activity of ESR1 in mare endometrium. This study offers new knowledge on the endometrial expression of ovarian steroids and OXT receptors in OXT pharmacologically induced luteal maintenance in the mare.
[Mh] Termos MeSH primário: Corpo Lúteo/efeitos dos fármacos
Cavalos/fisiologia
Ovário/fisiologia
Ocitocina/farmacologia
Prostaglandina-Endoperóxido Sintases/metabolismo
Receptores de Ocitocina/metabolismo
[Mh] Termos MeSH secundário: Animais
Corpo Lúteo/fisiologia
Estrogênios/genética
Estrogênios/metabolismo
Feminino
Ocitócicos/farmacologia
Progestinas/genética
Progestinas/metabolismo
Prostaglandina-Endoperóxido Sintases/genética
Receptores Estrogênicos/genética
Receptores Estrogênicos/metabolismo
Receptores de Ocitocina/genética
Receptores de Progesterona/genética
Receptores de Progesterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogens); 0 (Oxytocics); 0 (Progestins); 0 (Receptors, Estrogen); 0 (Receptors, Oxytocin); 0 (Receptors, Progesterone); 50-56-6 (Oxytocin); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28945805
[Au] Autor:Wang Y; Hu Y; He D; Chen S; Li S; Lan D; Ren P; Lin Z; Liu Y
[Ad] Endereço:Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu Campus, Chengdu, Sichuan, PR China.
[Ti] Título:Contribution of both positive selection and relaxation of selective constraints to degeneration of flyability during geese domestication.
[So] Source:PLoS One;12(9):e0185328, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Flyability is the most discrepant trait between modern-day geese and their wild ancestors, and the degeneration of flyability is a key marker of the successful domestication of wild geese. In light of the relatively short history of domestic geese, intense artificial selection is thought to play an important role in the degeneration of flyability. However, the underlying mechanism behind this phenomenon has seldom been investigated. In this study, we applied a molecular evolutionary approach to the evaluation of partial breeds of domestic geese in order to look for genes involved in the selection pressure toward degeneration of flyability. The haplotype networks, pairwise fixation index (FST) values, and analysis of molecular variance results all clearly illustrated a population variance between Landes geese and partial Chinese domestic geese. We also detected signatures of positive artificial selection in the COX2 and COX3 genes, and related selection in the HBB gene. Our results support the independent origins of partial European domestic geese and Chinese domestic geese. In addition, both positive artificial selection and the relaxation of functional constraints appeared to play important roles in the degeneration of flyability in domestic geese.
[Mh] Termos MeSH primário: Domesticação
Voo Animal/fisiologia
Gansos/genética
Gansos/fisiologia
Seleção Genética
[Mh] Termos MeSH secundário: Animais
Animais Domésticos
Animais Selvagens
Proteínas Aviárias/genética
Cruzamento
China
Ciclo-Oxigenase 2/genética
Europa (Continente)
Evolução Molecular
Variação Genética
Haplótipos
Hemoglobinas/genética
Prostaglandina-Endoperóxido Sintases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Avian Proteins); 0 (Hemoglobins); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); EC 1.14.99.1 (cyclooxygenase-3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185328


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[PMID]:28797264
[Au] Autor:Bijak M; Saluk-Bijak J
[Ad] Endereço:Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236, Lodz, Poland. michal.bijak@biol.uni.lodz.pl.
[Ti] Título:Flavonolignans inhibit the arachidonic acid pathway in blood platelets.
[So] Source:BMC Complement Altern Med;17(1):396, 2017 Aug 10.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Arachidonic acid metabolism by cyclooxygenase (COX) is a major pathway for blood platelets' activation, which is associated with pro-thrombotic platelet activity and the production of pro-inflammatory mediators. Inhibition of COX activity is one of the major means of anti-platelet pharmacotherapy preventing arterial thrombosis and reducing the incidence of cardiovascular events. Recent studies have presented that a silymarin (standardized extract of Milk thistle (Silybum marianum)) can inhibit the COX pathway. Accordingly, the aim of our study was to determine the effects of three major flavonolignans (silybin, silychristin and silydianin) on COX pathway activity in blood platelets. METHODS: We determined the effect of flavonolignans on arachidonic acid induced blood platelet aggregation, COX pathway metabolites formation, as well as COX activity in platelets. Additionally, we analysed the potential mechanism of this interaction using the bioinformatic ligand docking method. RESULTS: We observed that tested compounds decrease the platelet aggregation level, both thromboxane A and malondialdehyde formation, as well as inhibit the COX activity. The strongest effect was observed for silychristin and silybin. In our in silico study we showed that silychristin and silybin have conformations which interact with the active COX site as competitive inhibitors, blocking the possibility of substrate binding. CONCLUSIONS: The results obtained from this study clearly present the potential of flavonolignans as novel antiplatelet and anti-inflammatory agents.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Ácido Araquidônico/sangue
Plaquetas/efeitos dos fármacos
Cardo Mariano/química
Inibidores da Agregação de Plaquetas/farmacologia
Agregação Plaquetária/efeitos dos fármacos
Silimarina/farmacologia
[Mh] Termos MeSH secundário: Ligação Competitiva
Plaquetas/metabolismo
Flavonolignanos/farmacologia
Seres Humanos
Mediadores da Inflamação/sangue
Malondialdeído/sangue
Simulação de Acoplamento Molecular
Extratos Vegetais/farmacologia
Prostaglandina-Endoperóxido Sintases/sangue
Silimarina/química
Tromboxano A2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Flavonolignans); 0 (Inflammation Mediators); 0 (Plant Extracts); 0 (Platelet Aggregation Inhibitors); 0 (Silymarin); 27YG812J1I (Arachidonic Acid); 4RKY41TBTF (silybin); 4Y8F71G49Q (Malondialdehyde); 57576-52-0 (Thromboxane A2); 7P89L7W179 (silydianin); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); LK279ER14X (silychristin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1897-7


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[PMID]:28771028
[Au] Autor:Kaur G; Silakari O
[Ad] Endereço:Molecular Modeling Lab (MML), Department of Pharmaceutical Sciences & Drug Research, Punjabi University, Patiala, Punjab 147002, India.
[Ti] Título:Multiple target-centric strategy to tame inflammation.
[So] Source:Future Med Chem;9(12):1361-1376, 2017 Aug.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Single-target inhibition is an unsatisfactory therapeutic option to treat multifactorial pathologies, brought into limelight 'paradox of inflammation' beside dearth of innovation, rationalizes a shift toward 'multiple-target' design concept in anti-inflammatory research field. To improvise, two platform strategies, drugs mixture or multitarget drugs, are plausible. Dual cyclooxygenase/lipoxygenase inhibitor 'licofelone' developed after the backfire of rofecoxib due to safety concerns has fetched first light of triumph of the latter strategy. As hitting multiple targets in restraint is perhaps more viable strategy rather than single target, this review, outlines the most germane multiple target agents of synthetic and natural origin placing clear advantage in favors of multitarget strategy as real therapeutic solution for inflammation.
[Mh] Termos MeSH primário: Inibidores de Ciclo-Oxigenase/farmacologia
Inflamação/tratamento farmacológico
Lactonas/farmacologia
Inibidores de Lipoxigenase/farmacologia
Pirróis/farmacologia
Sulfonas/farmacologia
[Mh] Termos MeSH secundário: Inibidores de Ciclo-Oxigenase/síntese química
Inibidores de Ciclo-Oxigenase/química
Seres Humanos
Lactonas/síntese química
Lactonas/química
Lipoxigenase/metabolismo
Inibidores de Lipoxigenase/síntese química
Inibidores de Lipoxigenase/química
Estrutura Molecular
Prostaglandina-Endoperóxido Sintases/metabolismo
Pirróis/síntese química
Pirróis/química
Relação Estrutura-Atividade
Sulfonas/síntese química
Sulfonas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cyclooxygenase Inhibitors); 0 (Lactones); 0 (Lipoxygenase Inhibitors); 0 (Pyrroles); 0 (Sulfones); 0QTW8Z7MCR (rofecoxib); EC 1.13.11.12 (Lipoxygenase); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); P5T6BYS22Y (licofelone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0050


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[PMID]:28669741
[Au] Autor:Shrivastava SK; Srivastava P; Bandresh R; Tripathi PN; Tripathi A
[Ad] Endereço:Pharmaceutical Chemistry Research Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Electronic address: skshrivastava.phe@itbhu.ac.in.
[Ti] Título:Design, synthesis, and biological evaluation of some novel indolizine derivatives as dual cyclooxygenase and lipoxygenase inhibitor for anti-inflammatory activity.
[So] Source:Bioorg Med Chem;25(16):4424-4432, 2017 Aug 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Some novel indolizine derivatives were synthesized by bioisosteric modification of imidazo[1,2-a]pyridine for anti-inflammatory activity. The physicochemical characterization and structure of compounds were elucidated by state of the art spectroscopic technique. Induced fit docking was performed for initial screening to elucidate the interactions with corresponding amino acids of cyclooxygenase (COX-1, COX-2) and lipoxygenase (LOX) enzymes. The target compounds 53-60 were then evaluated against in vivo carrageenan and arachidonic acid induced rat paw edema models for anti-inflammatory activity. Amongst all the synthesized derivatives, compound 56 showed the significant anti-inflammatory activity in both rat paw edema models with very less ulcerogenic liability in comparison to standard diclofenac, celecoxib, and zileuton. The compounds 56 was further assessed to observe in vitro enzyme inhibition assay on both cyclooxygenase and lipoxygenase enzyme where it showed a preferential and selective non-competitive enzyme inhibition towards the COX-2 (IC =14.91µM, Ki=0.72µM) over COX-1 (IC >50µM) and a significant non-competitive inhibition of soybean lipoxygenase enzyme (IC =13.09µM, Ki=0.92µM). Thus, in silico, in vivo, and in vitro findings suggested that the synthesized indolizine compound 56 has a dual COX-2 and LOX inhibition characteristic and parallel in vivo anti-inflammatory activity in comparison to the standard drugs.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Inibidores de Ciclo-Oxigenase/farmacologia
Indolizinas/farmacologia
Inibidores de Lipoxigenase/farmacologia
Lipoxigenase/metabolismo
Prostaglandina-Endoperóxido Sintases/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/síntese química
Anti-Inflamatórios não Esteroides/química
Ácido Araquidônico
Carragenina
Inibidores de Ciclo-Oxigenase/síntese química
Inibidores de Ciclo-Oxigenase/química
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Desenho de Drogas
Edema/induzido quimicamente
Edema/tratamento farmacológico
Feminino
Indolizinas/síntese química
Indolizinas/química
Inibidores de Lipoxigenase/síntese química
Inibidores de Lipoxigenase/química
Masculino
Camundongos
Estrutura Molecular
Ratos
Relação Estrutura-Atividade
Úlcera/induzido quimicamente
Úlcera/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase Inhibitors); 0 (Indolizines); 0 (Lipoxygenase Inhibitors); 274-40-8 (indolizine); 27YG812J1I (Arachidonic Acid); 9000-07-1 (Carrageenan); EC 1.13.11.12 (Lipoxygenase); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE


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[PMID]:28637572
[Au] Autor:Sharpe JP; Khan NR; Chatterjee AR; Huang J; Magnotti LJ; Croce MA; Fabian TC
[Ti] Título:Investigating Cyclooxygenase Inhibition in a Rat Pulmonary Contusion Model: A Laboratory Study Finding No Improvement with Ibuprofen.
[So] Source:Am Surg;83(6):666-672, 2017 Jun 01.
[Is] ISSN:1555-9823
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Minimal advances have been made in the management of pulmonary contusions (PCs). The purpose of this study was to evaluate the impact of cyclooxygenase inhibition on outcomes following PC in a rat model. PC was induced in anesthetized adult rats. Ibuprofen was given to the treatment group (TG) and water was given to the control group (CG). Lung injury was assessed with pulse oximetry, arterial blood gases, CT, and histopathologic examination. Inflammation was measured with both serum and bronchoalveolar lavage (BAL) levels of tumor necrosis factor α and interleukin-6. Rats in the TG did not differ from rats in the CG with respect to oxygenation. Pathologic examination demonstrated a trend toward more inflammatory infiltrate in the CG, yet the sizes of the contusions were larger in the TG. The CG trended toward decreased levels of interleukin-6 in the serum and BAL at both three and seven days. While BAL levels of tumor necrosis factor α were increased in the TG at three days compared to the CG, they trended toward a reduced amount at seven days. Our data do not support cyclooxygenase inhibition for treatment to decrease the respiratory compromise associated with PC in this model of rat PCs.
[Mh] Termos MeSH primário: Contusões/metabolismo
Inibidores de Ciclo-Oxigenase/farmacologia
Ibuprofeno/farmacologia
Lesão Pulmonar
Prostaglandina-Endoperóxido Sintases
[Mh] Termos MeSH secundário: Animais
Lavagem Broncoalveolar
Contusões/patologia
Modelos Animais de Doenças
Inflamação/sangue
Inflamação/patologia
Interleucina-6/sangue
Pulmão/patologia
Oximetria
Oxigênio/metabolismo
Prostaglandina-Endoperóxido Sintases/efeitos dos fármacos
Ratos
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclooxygenase Inhibitors); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); S88TT14065 (Oxygen); WK2XYI10QM (Ibuprofen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE


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[PMID]:28515378
[Au] Autor:Sanaki T; Kasai-Yamamoto E; Yoshioka T; Sakai S; Yuyama K; Fujiwara T; Numata Y; Igarashi Y
[Ad] Endereço:Shionogi Innovation Center for Drug Discovery, Shionogi & Co., Ltd.
[Ti] Título:Direct Involvement of Arachidonic Acid in the Development of Ear Edema via TRPV3.
[So] Source:J Oleo Sci;66(6):591-599, 2017 Jun 01.
[Is] ISSN:1347-3352
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Arachidonic acid (AA) plays a pivotal role in the development of edema via its oxidized metabolites derived from cyclooxygenase (COX) and lipoxygenase (LOX), and is recently recognized as an activator of TRPV3. However, it is not clear whether AA plays some TRPV3-mediated pathological roles in the development of edema. Pharmacological and histological studies using ICR and ICR mice indicated that higher ear edema responses to topical application of AA were observed in ICR mice compared with ICR mice. However, there was no difference in the ear edema response to 12-O-tetradecanoylphorbol 13-acetate, skin histology, and skin barrier function between these mouse strains. Furthermore, oxidized fatty acids from the lesional site were analyzed to elucidate the TRPV3-mediated pathological roles of AA, and the results revealed that there were no differences in the level of COX or LOX metabolites derived from AA between both mouse strains. We concluded that AA plays a role in the development of TRPV3-mediated ear edema and that this result may contribute to better understanding of the pathophysiological mechanisms involved in the development of a certain type of edema.
[Mh] Termos MeSH primário: Ácidos Araquidônicos/efeitos adversos
Ácidos Araquidônicos/fisiologia
Otopatias/etiologia
Edema/etiologia
Canais de Cátion TRPV/fisiologia
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/metabolismo
Feminino
Lipoxigenase/fisiologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos ICR
Prostaglandina-Endoperóxido Sintases/fisiologia
Canais de Cátion TRPV/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (TRPV Cation Channels); 0 (Trpv3 protein, mouse); EC 1.13.11.12 (Lipoxygenase); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.5650/jos.ess16227


  10 / 13765 MEDLINE  
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[PMID]:28515072
[Au] Autor:Gong Y; Fu Z; Liegl R; Chen J; Hellström A; Smith LE
[Ad] Endereço:Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA; and.
[Ti] Título:ω-3 and ω-6 long-chain PUFAs and their enzymatic metabolites in neovascular eye diseases.
[So] Source:Am J Clin Nutr;106(1):16-26, 2017 Jul.
[Is] ISSN:1938-3207
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neovascular eye diseases, including retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration, threaten the visual health of children and adults. Current treatment options, including anti-vascular endothelial growth factor therapy and laser retinal photocoagulation, have limitations and are associated with adverse effects; therefore, the identification of additional therapies is highly desirable. Both clinical and experimental studies show that dietary ω-3 (n-3) long-chain polyunsaturated fatty acids (LC-PUFAs) reduce retinal and choroidal angiogenesis. The ω-3 LC-PUFA metabolites from 2 groups of enzymes, cyclooxygenases and lipoxygenases, inhibit [and the ω-6 (n-6) LC-PUFA metabolites promote] inflammation and angiogenesis. However, both of the ω-3 and the ω-6 lipid products of cytochrome P450 oxidase 2C promote neovascularization in both the retina and choroid, which suggests that inhibition of this pathway might be beneficial. This review summarizes our current understanding of the roles of ω-3 and ω-6 LC-PUFAs and their enzymatic metabolites in neovascular eye diseases.
[Mh] Termos MeSH primário: Retinopatia Diabética/metabolismo
Ácidos Graxos Ômega-3/metabolismo
Ácidos Graxos Ômega-6/metabolismo
Degeneração Macular/metabolismo
Retina/metabolismo
Neovascularização Retiniana/metabolismo
Retinopatia da Prematuridade/metabolismo
[Mh] Termos MeSH secundário: Sistema Enzimático do Citocromo P-450/metabolismo
Retinopatia Diabética/tratamento farmacológico
Ácidos Graxos Ômega-3/uso terapêutico
Ácidos Graxos Ômega-6/uso terapêutico
Seres Humanos
Lipoxigenases/metabolismo
Degeneração Macular/tratamento farmacológico
Prostaglandina-Endoperóxido Sintases/metabolismo
Retina/patologia
Doenças Retinianas/tratamento farmacológico
Doenças Retinianas/metabolismo
Neovascularização Retiniana/tratamento farmacológico
Retinopatia da Prematuridade/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fatty Acids, Omega-3); 0 (Fatty Acids, Omega-6); 0 (cytochrome P-450 CYP2C subfamily); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.13.11.- (Lipoxygenases); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.3945/ajcn.117.153825



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