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Phosphodiesterases
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Moritz Helmstädter, Manfred Schubert-Zsilavecz
It was noticed that PDE4 isoforms have a high level of expression in cells that regulate inflammatory responses and tissue remodelling such as most immune cells including macrophages, neutrophils, eosinophils and lymphocytes (Torphy, 1998; Korhonen et al., 2013). Early PDE4-selective inhibitors such as rolipram showed potent cAMP-mediated anti-inflammatory effects both in cellular and animal models which motivated pharmaceutical companies to invest a lot in developing PDE inhibitors for inflammation-related diseases such as asthma, COPD, allergic rhinitis and idiopathic pulmonary fibrosis. Experiments with carrageenan-induced paw inflammations show that rolipram increases the expression of mitogen-activated protein kinase phosphatase 1 (MKP-1). Additionally PDE4-Inhibitors suppress a variety of inflammatory responses including proliferation, chemotaxis, phagocytosis and release of pro-inflammatory mediators (Raker et al., 2016). Increased intracellular cAMP attenuates the expression of pro-inflammatory cytokines such as tumour necrosis factor alpha and leads to a higher production of anti-inflammatory cytokines such as interleukin-10. It also suppresses the expression of chemokines such as macrophage inflammatory protein 1a and 1b and suppresses the expression of pro-inflammatory lipid mediator leukotriene B4 (Serezani et al., 2008).
Imaging of Cardiovascular Disease
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Aleksandra Kalinowska, Lawrence W. Dobrucki
Active inflammatory cells produce a leukotriene B4 (LTB4) and secrete it as a potent chemotactic agent. In leukocytes, the leukotriene induces the adhesion and activation of the cells on the endothelium, while in neutrophils, LTB4 induces the formation of reactive oxygen species and the release of lysosome enzymes by these cells, contributing to the progression of inflammatory processes. Recently, a radiolabeled LTB4 receptor antagonist, 99mTc-RP517, has been developed for in vivo imaging of acute inflammation or infection. The tracer 99mTc-RP517 has a unique ability to label white blood cells in vivo after intravenous injection and has been noted to selectively localize to areas of inflammation (Serhan and Prescott 2000).
Fish oil supplementation fails to modulate indices of muscle damage and muscle repair during acute recovery from eccentric exercise in trained young males
Published in European Journal of Sport Science, 2023
Janna Mackay, Elena Bowles, Lewis J. Macgregor, Konstantinos Prokopidis, Christina Campbell, Eloise Barber, Stuart D. R. Galloway, Oliver C. Witard
Second, Ω3-PUFA ingestion has been proposed to enhance muscle repair by exerting anti-inflammatory properties. The incorporation of Ω3-PUFA into the muscle phospholipid bilayer occurs at the expense of Ω6-PUFA, forming the primary substrate for signalling pathways that regulate eicosanoid production catalysed by cyclooxygenase and lipoxygenase enzymes (Calder, 2017). This signalling cascade downregulates the formation of pro-inflammatory lipid mediators (prostaglandin E2/leukotriene B4) and upregulates lipid mediators with low pro-inflammatory potential (prostaglandin E3). Prostaglandin E3 stimulates blood flow and facilitates the repair of damaged tissues that is crucial for muscle remodelling following EIMD.