Effect of Boswellia serrata on intestinal motility in rodents: inhibition of diarrhoea without constipation

Authors


Department of Experimental Pharmacology, University of Naples Federico II, Via D. Montesano 49, 80131 Naples, Italy. E-mails: franborr@unina.it

Department of Experimental Pharmacology, University of Naples Federico II, Via D. Montesano 49, 80131 Naples, Italy. aaizzo@unina.it

Abstract

  • 1Clinical studies suggest that the Ayurvedic plant Boswellia serrata may be effective in reducing diarrhoea in patients with inflammatory bowel disease. In the present study, we evaluated the effect of a Boswellia serrata gum resin extract (BSE) on intestinal motility and diarrhoea in rodents.
  • 2BSE depressed electrically-, acetylcholine-, and barium chloride-induced contractions in the isolated guinea-pig ileum, being more potent in inhibiting the contractions induced by acetylcholine and barium chloride.
  • 3The inhibitory effect of BSE on acetylcholine-induced contractions was reduced by the L-type Ca2+ channel blockers verapamil and nifedipine, but not by the sarcoplasmic reticulum Ca2+-ATPase inhibitor cyclopiazonic acid, by the phosphodiesterase type IV inhibitor rolipram or by the lipoxygenase inhibitor zileuton.
  • 43-acetyl-11-keto-β-boswellic acid, one of the main active ingredients of B. serrata, inhibited acetylcholine-induced contractions.
  • 5BSE inhibited upper gastrointestinal transit in croton oil-treated mice as well as castor oil-induced diarrhoea. However, BSE did not affect intestinal motility in control mice, both in the small and in the large intestine.
  • 6It is concluded that BSE directly inhibits intestinal motility with a mechanism involving L-type Ca2+ channels. BSE prevents diarrhoea and normalizes intestinal motility in pathophysiological states without slowing the rate of transit in control animals. These results could explain, at least in part, the clinical efficacy of this Ayurvedic remedy in reducing diarrhoea in patients with inflammatory bowel disease.

British Journal of Pharmacology (2006) 148, 553–560. doi:10.1038/sj.bjp.0706740

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