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Nanodelivery Systems for NSAIDs: Challenges and Breakthroughs
Published in Ana Rute Neves, Salette Reis, Nanoparticles in Life Sciences and Biomedicine, 2018
José Lopes-de-Araújo, Catarina Pereira-Leite, Iolanda M. Cuccovia, Salette Reis, Claudia Nunes
Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most used medicines worldwide. For instance, approximately 30 million of US adults were regular users of NSAIDs in 2010 [1]. Such global use is supported by the remarkable efficacy of NSAIDs against inflammation, pain, and fever, which mainly arises from the inhibition of prostanoid biosynthesis through the cyclooxygenase (COX) pathway [2]. These pharmaceuticals are indicated for the relief of painful conditions (headache, menstrual pain, etc.) and for the treatment of chronic inflammatory diseases (osteoarthritis, rheumatoid arthritis [RA], etc.). Moreover, NSAIDs are available as prescription-only medicines and as over-the-counter preparations, being considered for short- or long-term therapies [3].
paniculata (C.B. Clarke) Munir Leaves on Various Gastric Aggressive Factors
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
P. S. Sreeja, K. Arunachalam, Parimelazhagan Thangaraj
Prostaglandins are small lipid molecules that have biological actions in various tissues and processes in the body, such as platelet aggregation, renal function, release of neurotransmitters, modulation of the immune response (Tarnawski et al. 2013), and an important role in the defense of the gastric mucosa. The endogenous prostaglandins originate from arachidonic acid through the oxidation by the constitutive COX-1, as well as by the induced isoform (COX-2); these are described as catalysts for the conversion of the arachidonic acid for the endoperoxide H2 (PGH2) and prostaglandin that serve as substrates for the biosynthesis of prostanoids (PGE2, PGF2α, PGD2, PGI2, and Thromboxane A2 (TXA2) (Hata and Breyer 2004).
Drug-induced bronchospasm
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
K Suresh Babu, Jaymin Morjaria
The basis of bronchospasm precipitated by aspirin and NSAIDs is based on the pharmacological inhibition of cyclooxygenase (COX) in arachidonic acid (AA) metabolism. Metabolism of arachidonic acid via the cyclooxygenase pathway leads to the generation of prostanoids, which are important signalling molecules produced during physiological as well as in inflammatory conditions. The airway inflammatory cells produce pro-inflammatory prostanoids PGD2 and PGF2α and antiinflammatory prostaglandins like PGE108,109
Biochanin A prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced adipocyte dysfunction in cultured 3T3-L1 cells
Published in Journal of Environmental Science and Health, Part A, 2019
Eun Mi Choi, Kwang Sik Suh, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Suk Chon
Arachidonic acid liberated by cPLA2 is metabolized by the COX system to prostanoids, which exert both pro- and anti-inflammatory effects.[42] The COX system consists of two distinct isozymes, the constitutive isoform (COX-1), which is responsible for maintaining normal physiological PG production, and the inducible form (COX-2), which accounts for upregulation of PG production in response to an inflammatory stimulus.[43] The cleavage of arachidonic acid from the sn-2 position of membrane glycerophospholipids by the action of highly selective cPLA2 is the initial and rate-limiting step in PG production, as well as a key step in the generation of other potent lipid messengers.[44] cPLA2 activity is tightly regulated by a post-translational mechanism involving mitogen-activated protein kinase/extracellular regulated kinase-dependent enzyme protein phosphorylation that facilitates translocation of the enzyme from the cytosol to the membrane, to gain access to phospholipid substrates.[45] COX-1 contributes to the rapid production of PGs in response to activation of cPLA2α.[46] In the present study, adding TCDD enhanced cPLA2 and COX-1 levels (Fig. 7) but not COX-2 levels (data not shown). These data demonstrate that the detrimental effects of TCDD on adipocytes are associated with an increase in PGE2 generation, controlled by the cPLA2/COX-1 enzyme system.
Ingestion of Sudan IV-adulterated palm oil impairs hepato-renal functions and induces the overexpression of pro-inflammatory cytokines: A sub-acute murine model
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Ofem E. Eteng, Ceaser A. Moses, Emmanuel I. Ugwor, Joe E. Enobong, Adio J. Akamo, Yewande Adebekun, Arikpo Iwara, Eyong Ubana
Inflammation, a component of the body’s intricate response to deleterious stimuli, such as xenobiotics and pathogens, is a defensive response involving several molecular mediators and the immune cells that secrete these mediators [30]. Mediators involved in the inflammatory process include the interleukins, TNF-α, CRP, and cyclooxygenases [30]. This study appraised the inflammatory response in the liver and kidneys following exposure to S4D-adulterated PO. In the liver, the expression of CRP and COX-2 were significantly elevated in the S4D-exposed groups. CRP is an acute-phase protein secreted predominantly by hepatocytes. CRP then binds to lysophosphatidylcholine present on the surface of dead or dying cells, thereby stimulating the immune system. Thus, the hepatic expression and therefore circulating levels of CRP are elevated during the inflammatory response [31]. Cyclooxygenases are enzymes concerned with the metabolism of arachidonic acid and biosynthesis of prostanoids, which are potent pro-inflammatory compounds [30]. While COX-1 is constitutively expressed in several tissues, the expression of COX-2 is inducible and becomes elevated during inflammation [32]. The elevated expression levels of CRP and COX-2, observed in this study, suggest that S4D dye invoked inflammation, in line with the study of [33]. This study reported that azo food dyes (sunset yellow, tartrazine, Allura red, and carmoisine) elicited cellular inflammatory responses and present potential health risks to the local population. On the other hand, liver expression of IL-10 was significantly repressed. IL-10 is an anti-inflammatory cytokine that predominantly inhibits the production of pro-inflammatory cytokines (e.g. TNFα and IL-1β) [34]. Thus, its repression further substantiates the postulated pro-inflammatory events instigated by S4D. The expression of BAX was also inhibited in the liver tissues of S4D-exposed rats, possibly alluding to its carcinogenic properties [13,35] since BAX is involved in p53-mediated apoptosis of aberrant cells and is inhibited in most carcinomas [36]. Moreover, the expression of acute-phase protein – CRP – was significantly elevated in the PO alone group. We attribute this inflammatory response to the rich saturated fatty acid (SFA) contents of PO, which are known initiators of inflammation via the TLR4/NFκB pathways [37]. However, the expressions of other mediators were comparable to the control, while the anti-inflammatory cytokine IL-10 was elevated in the PO alone group. The latter may be a compensatory response to check the possible inflammatory response elicited by the SFA in PO. However, its expression was progressively repressed as the concentration of S4D increased, suggesting a repressed anti-inflammatory response in the hepatic cells, in alignment with the elevated expression of CRP and COX-2 (both inflammatory mediators).