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The hallucinogenic herb Salvia divinorum and its active ingredient salvinorin A reduce inflammation-induced hypermotility in mice.

Raffaele Capasso, Francesca Borrelli, Jordan K Zjawiony, Lukasz Kutrzeba, Gabriella Aviello, G Sarnelli, F Capasso, Angelo A Izzo

Neurogastroenterology & Motility February 1, 2008 DOI: 10.1111/j.1365-2982.2007.00994.x (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Mice
Interventions salvinorin A U-50488 naloxone nor-binaltorphimine
Dose SDE 1-100 mg kg(-1); salvinorin A 0.01-10 mg kg(-1); U-50488 not specified; naloxone and nor-binaltorphimine not specified
Topics Salvia divinorum
Keywords Gut health Inflammation Gut motility
Citations 39
Key findings Salvinorin A inhibits gut motility in inflamed mice via KOR activation, but in healthy mice it does so only at high doses through a non-KOR mechanism.

Abstract

The hallucinogenic plant Salvia divinorum has been used for medical treatments of gastrointestinal disorders. Here, we evaluated the effect of a standardized extract from the leaves of Salvia divinorum (SDE) and of its active ingredient salvinorin A on motility in vivo, both in physiological states and during croton oil-induced intestinal inflammation. SDE (1-100 mg kg(-1)) significantly inhibited motility only in inflamed, but not in control, mice. In control mice, salvinorin A (0.01-10 mg kg(-1)) significantly inhibited motility only at the highest doses tested (3 and 10 mg kg(-1)) and this effect was not counteracted by naloxone or by the kappa-opioid receptor (KOR) antagonist nor-binaltorphimine. Inflammation significantly increased the potency of salvinorin A (but not of the KOR agonist U-50488) in reducing motility. The inhibitory effects of both salvinorin A and U-50488 in inflamed mice were counteracted by naloxone or by nor-binaltorphimine. We conclude that salvinorin A may reduce motility through activation of different targets. In physiological states, salvinorin A, at high doses, inhibited motility through a non-KOR mediated mechanism. Gut inflammation increased the potency of salvinorin A; this effect was mediated by KOR, but it was not shared by U-50488, thus suggesting that salvinorin A may have target(s) other than KOR in the inflamed gut.

Comparable studies

Other preclinical and animal studies on salvia divinorum, most cited first.

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