Abstract
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. 2. PEA significantly and dose-dependently decreased intestinal transit. The inhibitory effect of PEA (10 mg kg -1) was not modified by the cannabinoid CB 1 receptor antagonist SR141716A (0.3 mg kg -1, i.p.), the cannabinoid CB 2 receptor antagonist SR144528 (1 mg kg -1, i.p.), N G-nitro-L-arginine methyl ester (L-NAME, 25 mg kg -1, i.p.), yohimbine (1 mg kg -1, i.p.), naloxone (2 mg kg -1, i.p.) or hexamethonium (1 mg kg -1, i.p.). 3. PEA levels were significantly decreased in the small intestine of croton oil-treated mice. In these animals, PEA also inhibited motility and this effect was not counteracted by SR141716A (0.3 mg kg -1), or SR144528 (1 mg kg -1). 4. Pre-treatment of mice with the amidase inhibitor phenylmethyl sulphonil fluoride (PMSF, 30 mg kg -1, i.p.) did not modify the inhibitory effect of PEA, either in control or in mice with inflammation. 5. It is concluded that PEA inhibits intestinal motility with a peripheral mechanism independent from cannabinoid receptor activation. The decreased levels of PEA in croton oil-treated might contribute, at least in part, to the exaggerated transit observed during chronic intestinal inflammation.
| Original language | English |
|---|---|
| Pages (from-to) | 945-950 |
| Number of pages | 6 |
| Journal | British Journal of Pharmacology |
| Volume | 134 |
| Issue number | 5 |
| Publication status | Published - 2001 |
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Keywords
- Anandamide
- Cannabinoid receptors
- Fatty acid amide hydrolase
- Inflammatory bowel disease
- Intestinal motility
- Intestine
- Palmitoylethanolamide
ASJC Scopus subject areas
- Pharmacology
Cite this
Inhibitory effect of palmitoylethanolamide on gastrointestinal motility in mice. / Capasso, Raffaele; Izzo, Angelo A.; Fezza, Filomena; Pinto, Aldo; Capasso, Francesco; Mascolo, Nicola; Di Marzo, Vincenzo.
In: British Journal of Pharmacology, Vol. 134, No. 5, 2001, p. 945-950.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibitory effect of palmitoylethanolamide on gastrointestinal motility in mice
AU - Capasso, Raffaele
AU - Izzo, Angelo A.
AU - Fezza, Filomena
AU - Pinto, Aldo
AU - Capasso, Francesco
AU - Mascolo, Nicola
AU - Di Marzo, Vincenzo
PY - 2001
Y1 - 2001
N2 - 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. 2. PEA significantly and dose-dependently decreased intestinal transit. The inhibitory effect of PEA (10 mg kg -1) was not modified by the cannabinoid CB 1 receptor antagonist SR141716A (0.3 mg kg -1, i.p.), the cannabinoid CB 2 receptor antagonist SR144528 (1 mg kg -1, i.p.), N G-nitro-L-arginine methyl ester (L-NAME, 25 mg kg -1, i.p.), yohimbine (1 mg kg -1, i.p.), naloxone (2 mg kg -1, i.p.) or hexamethonium (1 mg kg -1, i.p.). 3. PEA levels were significantly decreased in the small intestine of croton oil-treated mice. In these animals, PEA also inhibited motility and this effect was not counteracted by SR141716A (0.3 mg kg -1), or SR144528 (1 mg kg -1). 4. Pre-treatment of mice with the amidase inhibitor phenylmethyl sulphonil fluoride (PMSF, 30 mg kg -1, i.p.) did not modify the inhibitory effect of PEA, either in control or in mice with inflammation. 5. It is concluded that PEA inhibits intestinal motility with a peripheral mechanism independent from cannabinoid receptor activation. The decreased levels of PEA in croton oil-treated might contribute, at least in part, to the exaggerated transit observed during chronic intestinal inflammation.
AB - 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. 2. PEA significantly and dose-dependently decreased intestinal transit. The inhibitory effect of PEA (10 mg kg -1) was not modified by the cannabinoid CB 1 receptor antagonist SR141716A (0.3 mg kg -1, i.p.), the cannabinoid CB 2 receptor antagonist SR144528 (1 mg kg -1, i.p.), N G-nitro-L-arginine methyl ester (L-NAME, 25 mg kg -1, i.p.), yohimbine (1 mg kg -1, i.p.), naloxone (2 mg kg -1, i.p.) or hexamethonium (1 mg kg -1, i.p.). 3. PEA levels were significantly decreased in the small intestine of croton oil-treated mice. In these animals, PEA also inhibited motility and this effect was not counteracted by SR141716A (0.3 mg kg -1), or SR144528 (1 mg kg -1). 4. Pre-treatment of mice with the amidase inhibitor phenylmethyl sulphonil fluoride (PMSF, 30 mg kg -1, i.p.) did not modify the inhibitory effect of PEA, either in control or in mice with inflammation. 5. It is concluded that PEA inhibits intestinal motility with a peripheral mechanism independent from cannabinoid receptor activation. The decreased levels of PEA in croton oil-treated might contribute, at least in part, to the exaggerated transit observed during chronic intestinal inflammation.
KW - Anandamide
KW - Cannabinoid receptors
KW - Fatty acid amide hydrolase
KW - Inflammatory bowel disease
KW - Intestinal motility
KW - Intestine
KW - Palmitoylethanolamide
UR - http://www.scopus.com/inward/record.url?scp=0035159492&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035159492&partnerID=8YFLogxK
M3 - Article
VL - 134
SP - 945
EP - 950
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 5
ER -