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Acta Physiologica Congress

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Acta Physiologica 2009; Volume 197, Supplement 672
The 60th National Congress of the Italian Physiological Society
9/23/2009-9/25/2009
Siena, Italy


EFFECT OF CANNABIDIOL, A NON-PSYCHOTROPIC COMPONENT OF CANNABIS SATIVA, ON INFLAMMATION-INDUCED INTESTINAL HYPERMOTILITY IN MICE
Abstract number: P152

SCALISI1 C, CAPASSO2 R, BORRELLI2 F, IZZO2 AA, FILECCIA1 R

1Dipartimento di Medicina Sperimentale - Sezione di Fisiologia Umana, Universit di Palermo
2Dipartimento di Farmacologia Sperimentale, Universit di Napoli Federico II(Italy)[email protected]

Aim: 

Cannabidiol (CBD), from Cannabis sativa, displays many actions, including antioxidant, neuroprotective, anticancer and anti-inflammatory properties. However, the pharmacological actions of cannabidiol in the digestive tract are largely unexplored. The aim of the present study is to assess the effect of CBD on intestinal motility in normal and in mice with intestinal inflammation.

Methods: 

Intestinal motility was evaluated by measuring the distribution of an orally-administered fluorescent marker along the small intestine. Intestinal inflammation was induced by the irritant croton oil.

Results: 

CBD had no effect on intestinal motility in control mice, but it significantly reduced the intestinal hypermotility associated to croton oil administration. The inhibitory effect of cannabidiol was counteracted by the cannabinoid CB1 receptor antagonist rimonabant (but not by the cannabinoid CB2 receptor antagonist SR144528) and by the fatty acid amide hydrolase (FAAH) inhibitor N-arachidonoyl-5-hydroxytryptamine (AA-5-HT).

Conclusions: 

Our results show that CBD normalize intestinal motility in an experimental model of ileitis and this effect involves indirect activation (via FAAH inhibition) of cannabinoid CB1 receptors. CBD might be considered as a good candidate for the treatment of hypermotility associated with inflammatory bowel disease.

To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 197, Supplement 672 :P152

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