Prophylactic efficacy of N-2-hydroxyethyl palmitamide (Impulsin®) in acute respiratory tract infections

Mašek, K.; Perlı́k, F; Klima, Jennifer; Kahlich, R

doi:10.1007/bf00560353

Cited by 36 publications

(26 citation statements)

References 10 publications

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“…Rather, PEA produces a well characterized series of analgesic and antiinflammatory effects in animals and humans, which are mediated by activation of PPAR-␣ receptors (Masek et al, 1974;Kahlich et al, 1979;Mazzari et al, 1996;Costa et al, 2002;Lo Verme et al, 2005;Kemeny et al, 2007;Genovese et al, 2008;Endocannabinoid Research Group et al, 2010). Nevertheless, the intrinsic roles of PEA in the response to proinflammatory triggers remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory Stimuli Control N-Acylphosphatidylethanolamine-Specific Phospholipase D Expression in Macrophages

Zhu¹,

Solórzano²,

Sahar³

et al. 2011

Molecular Pharmacology

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Palmitoylethanolamide (PEA) is an endogenous lipid amide that modulates pain and inflammation by engaging peroxisome proliferator-activated receptor type-␣. Here, we show that the proinflammatory bacterial endotoxin lipopolysaccharide (LPS) decreases PEA biosynthesis in RAW264.7 macrophages by suppressing the transcription of N-acylphosphatidylethanolamine-specific phospholipase D (NAPE-PLD), which catalyzes the production of PEA and other lipid amides. Using a luciferase reporter construct and chromatin immunoprecipitation, we further show that LPS treatment reduces acetylation of histone proteins bound to the NAPE-PLD promoter, an effect that is blocked by the histone deacetylase inhibitor trichostatin A. The transcription factor Sp1 is involved in regulating baseline NAPE-PLD expression but not in the transcriptional suppression induced by LPS. The ability of LPS to down-regulate PEA biosynthesis is impaired in peritoneal macrophages from mutant NAPE-PLD-deficient mice, in which PEA is produced through a compensatory mechanism distinct from NAPE-PLD. Moreover, NAPE-PLD-deficient mice fail to mount a normal inflammatory reaction in response to carrageenan administration in vivo. Our findings suggest that proinflammatory stimuli suppress NAPE-PLD expression and PEA biosynthesis in macrophages and that this effect might contribute to the inflammatory response.

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Section: Discussionmentioning

confidence: 99%

Proinflammatory Stimuli Control N-Acylphosphatidylethanolamine-Specific Phospholipase D Expression in Macrophages

Zhu¹,

Solórzano²,

Sahar³

et al. 2011

Molecular Pharmacology

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“…It is not clear what prompted these clinical trials; nonetheless, PEA was found to reduce the severity and duration of symptoms caused by the influenza virus in school children and soldiers (Kahlich et al, 1979;Masek et al, 1974). The apparent success of these trials led to the clinical use of PEA in the former Czechoslovakia for acute respiratory diseases during the late 1970s.…”

Section: Pea In the Clinicmentioning

confidence: 99%

The search for the palmitoylethanolamide receptor

et al. 2005

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Palmitoylethanolamide (PEA), the naturally occurring amide of ethanolamine and palmitic acid, is an endogenous lipid that modulates pain and inflammation. Although the anti-inflammatory effects of PEA were first characterized nearly 50 years ago, the identity of the receptor mediating these actions has long remained elusive. We recently identified the ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-a), as the receptor mediating the anti-inflammatory actions of this lipid amide. Here we outline the history of PEA, starting with its initial discovery in the 1950s, and discuss the pharmacological properties of this compound, particularly in regards to its ability to activate PPAR-a. Discovery of PEAThe discovery of naturally occurring fatty acid ethanolamides (FAEs) (Fig. 1) stems from an interesting clinical finding in the early 1940s, when investigators noted that supplementing the diets of 0024-3205/$ -see front matter D

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“…PEA was once used in the clinic to treat respiratory infections (Masek et al, 1974) and is currently utilized as a topical treatment for pruritus (Szepietowski et al, 2005). It exerts its anti-inflammatory and analgesic effects by activating the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-α) (LoVerme et al, 2005;LoVerme et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Synergistic antinociception by the cannabinoid receptor agonist anandamide and the PPAR-α receptor agonist GW7647

Russo

LoVerme

Rana

et al. 2007

European Journal of Pharmacology

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The analgesic properties of cannabinoid receptor agonists are well characterized. However, numerous side effects limit the therapeutic potential of these agents. Here we report a synergistic antinociceptive interaction between the endogenous cannabinoid receptor agonist anandamide and the synthetic peroxisome proliferator-activated receptor-α (PPAR-α) agonist 2-(4-(2-(1-Cyclohexanebutyl)-3-cyclohexylureido)ethyl)phenylthio)-2-methylpropionic acid (GW7647) in a model of acute chemical-induced pain. Moreover, we show that anandamide synergistically interacts with the largeconductance potassium channel (K Ca 1.1, BK) activator isopimaric acid. These findings reveal a synergistic interaction between the endocannabinoid and PPAR-α systems that might be exploited clinically and identify a new pharmacological effect of the BK channel activator isopimaric acid.

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Prophylactic efficacy of N-2-hydroxyethyl palmitamide (Impulsin®) in acute respiratory tract infections

Cited by 36 publications

References 10 publications

Proinflammatory Stimuli Control N-Acylphosphatidylethanolamine-Specific Phospholipase D Expression in Macrophages

Proinflammatory Stimuli Control N-Acylphosphatidylethanolamine-Specific Phospholipase D Expression in Macrophages

The search for the palmitoylethanolamide receptor

Synergistic antinociception by the cannabinoid receptor agonist anandamide and the PPAR-α receptor agonist GW7647

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