Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Anton C. de Groot in Monographs in Contact Allergy, 2021
Diclofenac is a benzeneacetic acid-derived nonsteroidal anti-inflammatory drug (NSAID) with antipyretic, antiinflammatory and analgesic actions. Its mechanism of action is as a cyclooxygenase inhibitor. Oral diclofenac is generally used to treat pain from dysmenorrhea, osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and from other causes. In pharmaceutical products, diclofenac is employed as diclofenac sodium (CAS number 15307-79-6, EC number 239-346-4, molecular formula C14H10Cl2NNaO2) (1). Diclofenac is also available in topical formulations including ointment, gel, suppositories, and as transdermal therapeutic system (TTS) for treatment of pain due to minor sprains, strains, and contusions (7,9). Lipid nanoemulsions of diclofenac may be used for parenteral applications.
Proinflammatory Peptides in Relation to Other Inflammatory Mediators
Sami I. Said in Proinflammatory and Antiinflammatory Peptides, 2020
The role of prostaglandins in the activation of sensory nerves induced by kinins merits specific attention. Three issues appear of particular relevance: first, bradykinin releases large amounts of prostaglandins from a variety of cells; second, prostaglandins are known to sensitize sensory nerves to the excitatory action of different mediators including kinins (25); and third, sensory neuropeptide release induced by bradykinin is markedly inhibited by indomethacin (26,27). Therefore, it appears that kinins and prostaglandins act synergistically to activate the dual afferent (pain transmission) and efferent functions (neuropeptide release) of primary sensory neurons. The ionic basis and the mechanism of release of sensory neuropeptides by prostaglandins and bradykinin has been reviewed recently (15). Kinins and prostaglandins are involved in the pathogenesis of painful and inflammatory diseases, including migraine and arthritis. In these pathologies, cyclooxygenase inhibitors have a major therapeutic impact. The therapeutic potential of the new peptide and nonpeptide antagonists of bradykinin B2 receptors will reflect the pathogenetic role played by kinins, but also how much of this role is independent from prostaglandin release.
Role of Eicosanoids in Renal Disease
Robin S. Goldstein in Mechanisms of Injury in Renal Disease and Toxicity, 2020
Numerous studies have explored the effect of cyclooxygenase inhibition on the proteinuria resulting from immune complex nephritis. Acute indomethacin treatment had no effect on established proteinuria induced by cationic bovine immunoglobulin, but it decreased renal blood flow (Rahman et al., 1987). In addition, treatment with salicylate exacerbated proteinuria in established immune complex nephritis (Kirschenbaum et al., 1985). Beneficial effects of cyclooxygenase inhibition have also been reported. Indomethacin treatment reduced proteinuria while having no effect on glomerular filtration rate in established glomerular nephritis induced by FxlA (Kirschenbaum et al., 1985) or gp330 (Zoja et al., 1987). Indomethacin also decreased proteinuria, glomerular filtration rate, and renal plasma flow in an isolated perfused kidney 2 h after FxlA exposure (Cybulsky et al., 1987).
Examining the correlation between salivary cytokine concentrations and CRP in people experiencing social-cognitive stress
Published in Neurological Research, 2023
Eric Chun Pu Chu, Anastasiya Spaska, Dimitar Monov, Mikhail Kasatkin, Natalia Stroiteleva
The pro-inflammatory cytokine IL-1ß has been pointed out to be an important mediator of the inflammatory response. The induction of cyclooxygenase-2 (Cox-2) by this cytokine can lead to inflammatory pain hypersensitivity. IL-1ß may play a causative role in migraine and cause neuroinflammation by inducing the expression of Cox-2 through the activation of neuronal and glial cells [26]. Another pro-inflammatory cytokine, IL-6, is secreted from T cells and macrophages to stimulate the immune response [21]. A high level of CRP may point to the pro-inflammatory status of patients with migraine and chronic TTH. The activation of the brain tissue leads to the release of peptides from the perivascular regions of the trigeminal nerve, causing inflammation and dilation of the extraparenchymal vessels [25].
Multimodal analgesia in neurosurgery: a narrative review
Published in Postgraduate Medicine, 2022
Caterina Aurilio, Maria Caterina Pace, Pasquale Sansone, Luca Gregorio Giaccari, Francesco Coppolino, Vincenzo Pota, Manlio Barbarisi
It is now understood that there are two forms of cyclooxygenase, termed cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is a constitutive isoform found in normal tissues, while COX-2 is induced in settings of inflammation and is constitutively expressed in certain areas of brain. NSAIDs are usually classified as mild analgesics, but it is important to consider the type of pain and its intensity in the assessment of analgesic efficacy. In postoperative pain, the NSAIDs may be superior to the opioids because they are particularly effective in different contests in which inflammation has caused sensitization of pain receptors [16]. The inhibition of COX-1 correlates with the inhibition of endogenous prostaglandins that impairs platelet function and promotes the ability of these drugs to increase the perioperative bleeding time. Probably for this reason, there are few clinical studies on the use of NSAIDs in brain surgery. In a Cochrane review, six studies were included in a meta-analysis on 742 patients to assess acute postoperative intensity of pain in brain surgery [10,17,18].
Protective effect of indomethacin on vanadium-induced adrenocortical and testicular damages in rat
Published in Toxicology Mechanisms and Methods, 2022
Rituparna Ghosh, Samudra Prosad Banik
Prostaglandins are distributed throughout the reproductive tract of the male and hold a key position in the common pathway through which hormones and drugs exert control over different aspects of reproduction. The enzymes cyclooxygenase (COX) catalyzes the first two steps in the biosynthesis of prostaglandins (PGs) from the substrate arachidonic acid. COX activity serves as an important rate limiting and commitment step in the prostaglandin synthesis pathway. Since the increase of prostaglandins attributes to the inflammatory response, nonsteroidal anti-inflammatory drugs (NSAIDS) reduce inflammation and pain by inhibiting the cyclooxygenase activities. There are two isoforms of the cyclooxygenase, COX-1 and COX-2 (Versteeg et al., 1999 ). COX-1 is a constitutively active enzyme that produces prostaglandins on the endoplasmic reticulum, which is then excreted and used for signaling purposes. COX-1 is expressed in various tissues at a constant level. The second isoform, COX-2 is normally absent in cells and is induced by growth factors, tumor promoters, or cytokines. In some tissue such as the brain, testes, and macula densa of the kidneys, COX-2 serves specialized functions, and is expressed regardless of stimulation. It is expressed in high concentration at sites of inflammation and in monocytes and macrophages (Vane and Botting 1998).
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