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Cyclooxygenase pathways

100%
Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.
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2014
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vol. 61
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issue 4
639-649
EN
This review compiles the current knowledge on the effects of prostanoids - arachidonic acid metabolites - on their own synthesis, activity and degradation. Interaction mechanisms between the receptors for the relevant compounds are presented, in particular with regard to the cooperation between a thromboxane A2 and prostaglandin I2 receptors. The questions of desensitization and internalization of receptors are discussed. The stages of the inflammatory response and tumor progression are analyzed against the background of the disruption of the synthesis of prostanoids. Special attention is given to the significance of 15-deoxy-Δ12,14-prostaglandin J2 in the regulation of the synthesis of prostanoids and its role as an anti-inflammatory agent. Ultimately, therapeutic approaches as used in various treatments are discussed in the light of the available knowledge.
2
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Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

75%
Pytlowany M., Strosznajder J., Jęśko H., Cąkała M., Strosznajder R.
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2008
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vol. 55
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issue 2
339-347
EN
Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (AA), a substrate for cyclo- and lipoxygenases (COX and LOX, respectively). In this study we investigated biochemical processes leading to cell death evoked by an NO donor, sodium nitroprusside (SNP). We found that SNP decreased viability of pheochromocytoma (PC12) cells in a concentration- and time-dependent manner. SNP at 0.1 mM caused a significant increase of apoptosis-inducing factor (AIF) protein level in mitochondria. Under these conditions 80% of PC12 cells survived. The enhancement of mitochondrial AIF level might protect most of PC12 cells against death. However, NO released from 0.5 mM SNP induced massive cell death but had no effect on protein level and localization of AIF and cytochrome c. Caspase-3 activity and poly(ADP-ribose) polymerase-1 (PARP-1) protein levels were not changed. However, PARP activity significantly decreased in a time-dependent manner. Inhibition of both COX isoforms and of 12/15-LOX significantly lowered the SNP-evoked cell death. We conclude that AIF, cytochrome c and caspase-3 are not responsible for the NO-mediated cell death evoked by SNP. The data demonstrate that NO liberated in excess decreases PARP-1 activity. Our results indicate that COX(s) and LOX(s) are involved in PC12 cell death evoked by NO released from its donor, SNP.
3
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Inflammation of the nasal mucosa and paranasal sinuses

75%
Woś J., Remjasz A.
Polski Przegląd Otorynolaryngologiczny
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2019
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vol. 8(1)
16-26
EN
Inflammation of the paranasal sinuses is a common condition that affects the upper respiratory tract. The pathomechanism and course of sinusitis are multifaceted, depending on the etiological factors, duration of the disease, anatomical abnormalities, and additional conditions exacerbating the inflammation of the nasal mucosa and paranasal sinuses. The gold standard of diagnostic imaging is computed tomography (CT), performed in particular cases. An auxiliary examination is a magnetic resonance imaging (MRI) for soft tissue imaging when there is a suspicion of a neoplastic process. The treatment of patients with rhinosinusitis is very complex and long-lasting, associated with the use of nasal or systemic corticosteroids, irrigation with physiological saline, as well as antibiotic therapy, antihistamines or herbal supplements. The treatment is selected individually for the patient's condition or the sinus phenotype, and in exceptional cases, surgical intervention is undertaken. Work is continuing on genetic, molecular and immunological research to search for new and effective methods of treatment of rhinosinusitis.
4
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Wybrane aspekty bezpieczeństwa leczenia NLPZ

63%
Rell K.
Pediatria i Medycyna Rodzinna
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2011
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vol. 7
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issue 1
41-48
EN
Non-steroidal anti-inflammatory drugs (NSAIDs) are, besides paracetamol, the cornerstone of therapy of mild and moderate pain, particularly in acute and chronic conditions of musculoskeletal system. They are also a valuable adjunct in the management of severe pain by opioid derivates. However, their widespread use and over-the-counter availability of selected preparations contribute to a high incidence of adverse effects. The main mechanism of action of NSAIDs is associated with reduced activity of cyclooxygenase (COX). Selective compounds predominantly affect the COX-2, while “classic” ones inhibit both COX-1 and COX-2 to a similar degree. This influences the incidence of adverse effects during their use. Selective NSAIDs contribute more to an increased cardiovascular risk, than to gastrointestinal complications. Among “classic” NSAIDs, diclofenac is the most selective and thus associated with the highest risk of cardiovascular complications. The incidence depends also on duration of treatment and dosage regimen. Non-selective preparations appear safer for the cardiovascular system. According to cardiological recommendations, in patients at high risk of cardiovascular complications, naproxen should be considered the first-line drug, devoid of any COX-2 selectivity. Risk of damage of the digestive tract by these drugs may be reduced by concomitant use of proton pump inhibitors. The greatest risk of severe liver damage resulting in organ failure and death, has been correlated with nimesulide, resulting in a considerable limitation of indications by manufacturers. At present, nimesulide may be administered only as a second-line drug, when other NSAIDs proved ineffective and several contraindications were excluded. Topical application of NSAIDs may improve penetration of drugs to poorly vascularised tissues. In this setting, transdermal administration of ketoprofen proved highly effective.
PL
Niesterydowe leki przeciwzapalne (NLPZ) są obok paracetamolu podstawowymi lekami stosowanymi w terapii bólu łagodnego i umiarkowanego, szczególnie w ostrych i przewlekłych chorobach narządu ruchu. Stanowią także cenne uzupełnienie w leczeniu silnego bólu lekami opioidowymi. Ich bardzo szerokie rozpowszechnienie i dostępność niektórych preparatów bez recepty wiąże się jednak z dużą częstością objawów niepożądanych. Główny mechanizm działania NLPZ polega na zmniejszeniu aktywności cyklooksygenazy (COX). Preparaty selektywne silniej działają na cyklooksygenazę COX-2, a tzw. „klasyczne” w zbliżonym stopniu na COX-1 i COX-2. Ma to wpływ na częstość objawów niepożądanych podczas stosowania tych leków. Selektywne NLPZ w większym stopniu zwiększają ryzyko sercowo-naczyniowe, a w mniejszym ryzyko gastryczne. Wśród tzw. „klasycznych” NLPZ największą selektywność i największe ryzyko powikłań sercowo-naczyniowych wykazuje diklofenak. Częstość powikłań zależy od czasu leczenia oraz dawki stosowanego leku. Preparaty bez selektywności względem COX-2 wydają się bezpieczniejsze dla układu sercowo-naczyniowego. Według zaleceń kardiologicznych u pacjentów wysokiego ryzyka sercowo- naczyniowego lekiem z wyboru powinien być naproksen, który nie wykazuje selektywności względem COX-2. Ryzyko uszkodzenia przewodu pokarmowego po tych lekach można zmniejszyć poprzez stosowanie inhibitorów pompy protonowej (IPP). Największe ryzyko ciężkiego uszkodzenia wątroby z jej niewydolnością i przypadkami zgonów opisywano po nimesulidzie, którego stosowanie zostało ograniczone przez producentów leku. Nimesulid może być obecnie przepisywany jedynie jako lek drugiego rzutu, po stwierdzeniu nieskuteczności innych NLPZ i wykluczeniu wielu przeciwwskazań. Podawanie miejscowe preparatów NLPZ może zwiększać penetrację leków do gorzej unaczynionych tkanek. Dużą skuteczność wykazano dla podawanego przezskórnie ketoprofenu.
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