The hallucinogenic herb Salvia divinorum and its active ingredient salvinorin A reduce inflammation-induced hypermotility in mice.
R Capasso, F Borrelli, J Zjawiony, L Kutrzeba, G Aviello, G Sarnelli, F Capasso, A A Izzo
Neurogastroenterology and Motility February 1, 2008 DOI: 10.1111/j.1365-2982.2007.00994.x (opens in new tab) via PubMed
Summary
AI-generated from the abstractAn extract from the hallucinogenic plant Salvia divinorum and its active ingredient salvinorin A reduce gut motility in mice, but only during intestinal inflammation. In healthy mice, salvinorin A slowed motility only at high doses, and this effect did not involve kappa-opioid receptors (KOR). Inflammation made salvinorin A more potent at lower doses, and this effect was blocked by KOR antagonists, indicating a switch to KOR-mediated action. A standard KOR agonist did not share this enhanced potency, suggesting salvinorin A may act through additional targets in the inflamed gut.
Study at a glance
| 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 finding | 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.