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cyclooxygenase/carie dentaire
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Expression of cyclooxygenase-1 and -2 is limited to the nasal glands in the guinea pig nasal cavity.
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OBJECTIVE
To clarify the localization of cyclooxygenase (COX)-1 and -2 in the nasal cavity of guinea pigs and ascertain their physiological roles.
METHODS
The distribution of the enzymes was investigated using immunohistochemistry.
RESULTS
Immunoreactivities for COX-1 and -2 were limited to the
Immunohistochemical study on overexpression of cyclooxygenase-2 in squamous cell carcinoma of the oral cavity: its importance as a prognostic predictor.
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Cyclooxygenase-2 (COX-2) is known as one of the critical prognostic factors in carcinomas of the various organs. However, the importance of COX-2 overexpression in oral squamous cell carcinomas has not been fully described yet. We investigated overexpression of COX-2 by immunohistochemistry in 72
Expression of cyclooxygenase genes and involvement of endogenous prostaglandin during osteogenesis in the rat tibial bone marrow cavity.
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Many researchers have demonstrated that the administration of prostaglandins (PGs), especially PGE2, increases the bone volume in vivo. It is still not clear how endogenous PG is associated with such bone formation. Cyclooxygenase (COX), which acts in the synthesis of PG from arachidonic acid, has
Cyclooxygenase-2 expression in squamous cell carcinoma of the oral cavity and pharynx: association to p53 and clinical outcome.
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Cyclooxygenase-2 (COX-2) expression is up-regulated in transformed cells and in malignant tissues, including tumours of the head and neck, and it has prognostic significance in many types of cancer. COX-2 expression is suppressed by the wild-type but not by the mutant tumour suppressor gene TP53.
Cyclooxygenase inhibitors induce apoptosis in oral cavity cancer cells by increased expression of nonsteroidal anti-inflammatory drug-activated gene.
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We have investigated whether NAG-1 is induced in oral cavity cancer cells by various NSAIDs and if apoptosis induced by NSAIDs can be linked directly with the induction of NAG-1. NAG-1 expression was increased by diclofenac, aceclofenac, indomethacin, ibuprofen, and sulindac sulfide, in the order of
Cyclooxygenase-2 is a possible target of treatment approach in conjunction with photodynamic therapy for various disorders in skin and oral cavity.
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BACKGROUND
Anti-cancer effects of cyclooxygenase (COX)-2 inhibitors have been reported, but not fully investigated in skin and oral diseases. 5-aminolaevulinic acid (ALA)-based photodynamic therapy (PDT) for treating those patients with skin and oral lesions is a highly sophisticated procedure, but
Enzyme selectivity of new cyclooxygenase-2/5 lipoxygenase inhibitors using molecular modeling approach.
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We have studied the conformational flexibility of three 5-keto-substituted 7-tert-butyl-2,3-dihydro-3,3-dimethylbenzofurans (DHDMBFs) which show dual cyclooxygenase (COX) and 5-lipoxygenase (LOX) inhibition and are potential candidates as antiinflammatory agents and analgesics. The conformations
Computer simulation of the interaction of non-steroidal anti-inflammatory drugs: indoprofen and NS398 with cyclooxygenase.
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We have applied computer simulation technique to study interaction of two anti-inflammatory drugs (NSAIDs) indoprofen and NS398 with cyclooxygenase (COX-1 and COX-2) enzymes. We have also investigated conformational flexibility of the two drugs by systematic search and simulated annealing molecular
Hot-spots-guided receptor-based pharmacophores (HS-Pharm): a knowledge-based approach to identify ligand-anchoring atoms in protein cavities and prioritize structure-based pharmacophores.
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The design of biologically active compounds from ligand-free protein structures using a structure-based approach is still a major challenge. In this paper, we present a fast knowledge-based approach (HS-Pharm) that allows the prioritization of cavity atoms that should be targeted for ligand binding,
Elevated interleukin 6 is induced by prostaglandin E2 in a murine model of inflammation: possible role of cyclooxygenase-2.
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Injection of mineral oils such as pristane into the peritoneal cavities of BALB/c mice results in a chronic peritonitis associated with high tissue levels of interleukin 6 (IL-6). Here we show that increased prostaglandin E2 (PGE2) synthesis causes induction of IL-6 and that expression of an
Differential involvement of cyclooxygenase isoforms in neutrophil migration in vivo and in vitro.
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Pretreatment using celecoxib, a cyclooxygenase (COX) 2 inhibitor, or indomethacin, a nonselective COX inhibitor, reduced lypopolyssaccharide (LPS)-induced leukocyte migration to the rat peritoneal cavity. The effect of celecoxib (12 mg/kg) or indomethacin (2 mg/kg) on neutrophil chemotaxis induced
Local and systemic expression of inducible nitric oxide synthase in comparison with that of cyclooxygenase-2 in rat carrageenin-induced pleurisy.
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Expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) is up-regulated in response to inflammatory stimuli. To evaluate the extent to which local pleural inflammation involves additional site in the pleural cavity and elsewhere, we investigated the time course of the
Cyclooxygenase-2 deficiency in macrophages leads to defective p110γ PI3K signaling and impairs cell adhesion and migration.
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Cyclooxygenase (Cox)-2 dependent PGs modulate several functions in many pathophysiological processes, including migration of immune cells. In this study, we addressed the role of Cox-2 in macrophage migration by using in vivo and in vitro models. Upon thioglycolate challenge, CD11b(+) F4/80(+)
Accelerated hematopoietic recovery and protective effect of the cyclooxygenase inhibitor indomethacin in bacterial infection of neutropenic mice.
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The effects of indomethacin administration on Pseudomonas aeruginosa infection were investigated in neutropenic mice. Cyclophosphamide-treated mice received the drug at 2.5 to 12 mg/kg according to different regimens, to be challenged with a lethal intraperitoneal inoculum of P. aeruginosa 5 days
Comparative expression of cyclooxygenase 2 and Ki67 in amelanotic and conventional oral melanomas.
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