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Chemical Compound Review

C18-PAF     2-[[(2R)-2-acetyloxy-3- octadecoxy-propoxy]...

Synonyms: CHEMBL1788194, CHEBI:75217, PAF C18, AC1MBZ4F, BML3-E05, ...
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Disease relevance of PAF acether


High impact information on PAF acether

  • The latter appeared to be involved in the inhibition of proinflammatory cytokine production because addition of exogenous TGF-beta1, prostaglandin E2, or PAF resulted in inhibition of lipopolysaccharide-stimulated cytokine production [6].
  • The objective of this study was to determine if the enhanced leukocyte adherence and emigration associated with inhibition of NO production involves inflammatory agents such as platelet-activating factor (PAF) and leukotriene B4 (LTB4) and/or phospholipase A2 (PLA2) [7].
  • Spermine-NO prevented the mast cell-dependent neutrophil adhesion but failed to affect direct adhesion with PAF [8].
  • Because of the structural similarities between PAF and the truncated phosphatidylcholines (polar PCs) generated during lipoprotein oxidation, we investigated the possibility that LCAT may also hydrolyze polar PCs to lyso-PC during the oxidation of plasma [9].
  • We used eNOS-deficient (eNOS-/-) mice and their wild-type control as experimental animals, platelet-activating factor (PAF) at 10(-7) m as the test pro-inflammatory agent, and integrated optical intensity (IOI) as an index of microvascular permeability [10].

Chemical compound and disease context of PAF acether


Biological context of PAF acether

  • 111In-eosinophil accumulation induced by PAF and in the PCA reaction was also inhibited by L-NAME but not by D-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)[16]
  • PAF has been proposed to be a retrograde messenger of long-term potentiation (LTP): the antagonist of PAFRs, ginkgolide B (or BN52021) prevents induction of LTP [17].
  • Significant inhibition (45%) of PAF-release was obtained with 50 microM cloricromene and the IC50 was 85 microM [18].
  • 3. I.v. administration of PAF induced a small accumulation of 111indium-labelled neutrophils within the pulmonary circulation which could be greatly potentiated by pretreatment of the animals with L-NAME [19].
  • 4. The present findings indicate that inhibition of endogenous NO synthesis leads to an increase in protein extravasation and to potentiation of the permeability effects of PAF and endothelin-1 in the coronary circulation [20].

Anatomical context of PAF acether

  • In addition to IFN-gamma, chemoattractant molecules, such as platelet-activating factor (PAF) and CC chemokines, may also activate macrophages to induce NO and mediate the killing of T. cruzi in an NO-dependent manner [21].
  • Similarly, PAF increased IOI in the mesentery of wild-type mice but much less in the mesentery of eNOS-/- mice [10].
  • 111In-labelled eosinophil accumulation induced by platelet-activating factor (PAF) and zymosan-activated plasma (as a source of C5a des Arg) was also inhibited [22].
  • As a control we used plasma extravasation induced by platelet activating factor (PAF), which acts directly on the endothelium of the blood vessels, that is, its action is independent of any innervation [23].
  • Incubation of EC with histamine or PAF for 1 h resulted in a four- to eight-fold decrease of beta-adrenoreceptor density in the plasma membranes [24].

Associations of PAF acether with other chemical compounds


Gene context of PAF acether

  • Previous studies of crystal structures of GM2AP complexed with the physiological ligand GM2 and platelet activating factor (PAF) have shown binding at two specific locations within the spacious apolar pocket and an ordering effect of endogenous resident lipids [29].
  • The induction of iNOS is mediated by the release of endogenous tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and PAF by endotoxin [30].
  • In the earlier phases of shock, activation of the endothelial, constitutive NOS (ecNOS) occurs, which, in the case of endotoxic shock, is triggered by endotoxin-induced, acute release of platelet-activating factor (PAF) and also other potential mediators [30].
  • In alpha-toxin-permeabilized PMNs, AA release and PAF production result from the specific activation of cytosolic PLA2 (cPLA2) [31].
  • PAF increased IOI to comparable values in the mesenteries of wild-type mice and those lacking the gene for inducible NOS (iNOS) [10].

Analytical, diagnostic and therapeutic context of PAF acether

  • Perfusion with PAF (10 nM) induced a robust transient high Lp [24.3 +/- 1.7 x 10-7 cm/(s.cmH2O)] that peaked in 8.9 +/- 0.5 min and then returned toward control Lp [1.6 +/- 0.1 x 10-7 cm/(s.cmH2O)] [32].
  • Reconstruction of venular segments with the use of transmission electron microscopy of serial sections confirmed that PAF induces paracellular inflammatory gaps [32].
  • 5. Electrical stimulation of the lumbar sympathetic chain at frequencies of 0.25-5 Hz, which probably also significantly decreases blood flow through the joint capsule, reduced basal plasma extravasation, BK-induced PE and PAF-induced PE [23].
  • In conclusion, PGE2 and PAF, and ligation of VnR as well, contribute to amplify viral growth in HIV-1-infected macrophages upon uptake of apoptotic cells [33].
  • The stimulation of cyclic GMP synthesis induced by PAF was dose-dependent and was suppressed after treatment with PCA-4248, a PAF antagonist, a fact that could suggest the involvement of specific PAF receptors [34].


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  15. Effect of SRI 63-675 on hemodynamics and blood PAF levels during porcine endotoxemia. Dobrowsky, R.T., Voyksner, R.D., Olson, N.C. Am. J. Physiol. (1991) [Pubmed]
  16. Role of prostaglandins and nitric oxide in acute inflammatory reactions in guinea-pig skin. Teixeira, M.M., Williams, T.J., Hellewell, P.G. Br. J. Pharmacol. (1993) [Pubmed]
  17. Inhibition of hippocampal LTP by ginkgolide B is mediated by its blocking action on PAF rather than glycine receptors. Kondratskaya, E.L., Pankratov, Y.V., Lalo, U.V., Chatterjee, S.S., Krishtal, O.A. Neurochem. Int. (2004) [Pubmed]
  18. Inhibition of PAF synthesis by stimulated human polymorphonuclear leucocytes with cloricromene, an inhibitor of phospholipase A2 activation. Ribaldi, E., Mezzasoma, A.M., Francescangeli, E., Prosdocimi, M., Nenci, G.G., Goracci, G., Gresele, P. Br. J. Pharmacol. (1996) [Pubmed]
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  33. Interaction of macrophages with apoptotic cells enhances HIV Type 1 replication through PGE2, PAF, and vitronectin receptor. Lima, R.G., Moreira, L., Paes-Leme, J., Barreto-de-Souza, V., Castro-Faria-Neto, H.C., Bozza, P.T., Bou-Habib, D.C. AIDS Res. Hum. Retroviruses (2006) [Pubmed]
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