Disease relevance of Impulsin

• Anandamide and palmitoylethanolamide significantly reduced this hyperalgesia [1].
• Idiopathic infertility: effect of palmitoylethanolamide (a homologue of anandamide) on hyperactivated sperm cell motility and Ca2+ influx [2].
• N-(2-hydroxyethyl)hexadecanamide is orally active in reducing edema formation and inflammatory hyperalgesia by down-modulating mast cell activation [3].
• Changes in endocannabinoid and palmitoylethanolamide levels in eye tissues of patients with diabetic retinopathy and age-related macular degeneration [4].
• A possible explanation of the mechanism by which Impulsin decreased the toxicity of virus in the organism is discussed [5].

High impact information on Impulsin

• RESULTS: Motility was inhibited by N-arachidonoylserotonin (AA-5-HT) and palmitoylisopropylamide, 2 selective FAAH inhibitors, as well as by the FAAH substrates palmitoylethanolamide, oleamide, and oleoylethanolamide [6].
• Cannabinoids, which like palmitoylethanolamide are functionally active at the peripheral cannabinoid receptor CB2 on mast cells, also prevented neuron loss in this delayed postglutamate model [7].
• Analogous pharmacological behaviors have been observed for palmitoylethanolamide (ALI-Amides) in downmodulating mast cell activation [7].
• Other endocannabinoids such as 2-arachidonoylglycerol, linoleoylethanolamide, oleoylethanolamide, and palmitoylethanolamide did not promote cell death under the same experimental conditions [8].
• The nuclear receptor peroxisome proliferator-activated receptor-alpha mediates the anti-inflammatory actions of palmitoylethanolamide [9].

Chemical compound and disease context of Impulsin

• Attempt to influence silicotic fibrosis by means of N-(2-hydroxyethyl) palmitamide (Impulsin) [10].

Biological context of Impulsin

• Beta-NGF-induced HBCC proliferation was potently inhibited (IC50 = 50-600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190 [11].
• 1. The ability of a series of homologues and analogues of palmitoylethanolamide to inhibit the uptake and fatty acid amidohydrolase (FAAH)-catalysed hydrolysis of [(3)H]-anandamide ([(3)H]-AEA) has been investigated [12].
• After 4 days of treatment, AEA and 2-AG inhibited C6 cell proliferation with similar potencies (IC(50) values of 1.6 and 1.8 microM, respectively), whereas palmitoylethanolamide showed no significant antiproliferative effects at concentrations up to 10 microM [13].
• Inhibitory effect of palmitoylethanolamide on gastrointestinal motility in mice [14].
• HU-210 (30 microM), a synthetic CB1 receptor agonist, and palmitoylethanolamide (30 microM), a CB2 receptor agonist, did not influence the membrane potential of the vascular smooth muscle cells [15].

Anatomical context of Impulsin

• On the basis of this as well as previous findings it is now possible to hypothesize for AnNH and palmitoylethanolamide, co-synthesized by macrophages, a role as peripheral mediators with multiple actions on blood cell function [16].
• Only palmitoylethanolamide reduced neutrophil influx [1].
• Pharmacological properties of rat brain fatty acid amidohydrolase in different subcellular fractions using palmitoylethanolamide as substrate [17].
• Palmitoylethanolamide, a selective CB(2) receptor agonist, did not relax precontracted coronary arteries [18].
• Palmitoylethanolamide, palmitoylisopropylamide and R-palmitoyl-(2-methyl)ethanolamide had modest effects upon [(3)H]-CP 55,940 binding to human CB(1) receptors expressed on CHO cells [12].

Associations of Impulsin with other chemical compounds

• The anti-hyperalgesic actions of the cannabinoid anandamide and the putative CB2 receptor agonist palmitoylethanolamide in visceral and somatic inflammatory pain [19].
• Finally, as previously shown in central neurons, on stimulation with ionomycin, J774 macrophages also produced a mixture of AEs including AnNH and palmitoylethanolamide, which has been proposed as the preferential endogenous ligand at the peripheral cannabinoid receptor CB2 and, consequently, as a possible down-modulator of mast cells [16].
• 2. Among the endocannabinoid molecules tested, anandamide (AEA), but not 2-arachidonoyl-glycerol (2-AG) or palmitoyl-ethanolamide (PEA), increased the intracellular fluorescence emitted by calcein, a metabolic derivative of the P-gp substrate calcein-AM, indicative of a reduction in transport capacity [20].
• HMC-1 cells did not display a functional cannabinoid receptor on their surface and neither AEA nor palmitoylethanolamide affected tryptase release from these cells [21].
• We have investigated the inhibition of lipopolysaccharide stimulated nitric oxide production in RAW264.7 macrophages by the cannabinoids and the putative cannabinoid CB(2)-like receptor ligand, palmitoylethanolamide [22].

Gene context of Impulsin

• FAAH (K(m)=5.0+/-0.5 microM, V(max)=160+/-15 pmol min(-1) mg protein(-1)) was competitively inhibited by palmitoylethanolamide [21].
• The endocannabinoid circuit involves two cloned receptors: CB1 in the CNS and CB2 in the periphery; endogenously produced ligands including anandamide, 2-arachidonylglycerol and palmitoylethanolamide; and enzymes that degrade endocannabinoid ligands to terminate signaling [23].
• The endogenous cannabinoid anandamide, but not the CB2 ligand palmitoylethanolamide, prevents the viscero-visceral hyper-reflexia associated with inflammation of the rat urinary bladder [24].
• In human embryonic kidney cells over-expressing the human vanilloid receptor type 1 (VR1), palmitoylethanolamide (PEA, 0.5-10 microM) enhanced the effect of arachidonoylethanolamide (AEA, 50 nM) on the VR1-mediated increase of the intracellular Ca2+ concentration [25].
• 7. It is concluded that although palmitoylethanolamide has entourage-like effects at VR1 receptors expressed on hVR1-HEK293 cells, other N-acyl ethanolamines have even more dramatic potentiating effects [26].

Analytical, diagnostic and therapeutic context of Impulsin

• 2. Dose-response curves for coronary perfusion pressure (CPP) and LVDP were constructed to anandamide, R-(+)-methanandamide, palmitoylethanolamide (PEA) and JWH015 in isolated Langendorff-perfused rat hearts [27].
• 1. We have studied the effect of palmitoylethanolamide (PEA, 2.5 - 30 mg kg(-1), i.p.) on upper gastrointestinal transit in control mice and in mice with chronic intestinal inflammation induced by croton oil [14].
• Early studies investigating the effects of palmitoylethanolamide on animal models of inflammation and on rat mast cells led to the hypothesis that endogenous cannabinoids might act as local autacoids which suppressed inflammation by reducing the activation of mast cells [28].
• The diurnal variations of the endocannabinoid arachidonoylethanolamine (anandamide, ANA) as well as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) were detected and quantified in cerebrospinal fluid (CSF), pons, hippocampus, and hypothalamus in the rat over 24 h using HPLC/MS [29].
• The effect of long-term administration of N-(2-hydroxyethyl)palmitamide on the chemotherapy of RBA rat leukemia [30].

References