Activation of the cannabinoid 2 receptor (CB2) protects against experimental colitis

Abstract

Background-Activation of cannabinoid (CB) 1 receptors results in attenuation of experimental colitis. Our aim was to examine the role of CB 2 receptors in experimental colitis using agonists (JWH133, AM1241) and an antagonist (AM630) in trinitrobenzene sulfonic acid (TNBS)-induced colitis in wildtype and CB 2 receptor-deficient (CB 2 -/-) mice.

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

“…Recently, Gertsch et al 23 reported that BCP is a CB2 agonist. CB2 is expressed mainly in immune cells, and its activation limits intestinal inflammation 30 and reduces proinflammatory mediator release. 67 The present study demonstrated that the anti-inflammatory effect of BCP was almost completely reversed by the selective CB2 antagonist AM630, strongly suggesting that a great part of the anti-inflammatory properties of BCP observed in DSS-induced colitis was mediated by CB2 activation.…”

The endocannabinoid system in inflammatory bowel diseases: from pathophysiology to therapeutic opportunity

“…Indeed, CB 1 expression was increased in the myenteric plexuses of DNBS-mice, owing to an increase in cells expressing CB 1 , with no change in the overall neuronal population [50], whereas no difference was observed in CB 1 mRNA expression in the colon of TNBS-mice [57]. CB 2 expression, by contrast, was increased in one study of DSS-induced colitis and TNBS mice [61] but unchanged in a second study of TNBS mice [57].…”

“…AM1241 (10 mg/kg or 20 mg/kg, b.i.d. ), a CB 2 agonist, was used in the context of TNBS-induced colitis with the same outcome as JWH-133 [61]. The effects of both agonists were confirmed to be CB 2 -mediated because they were reversed in the presence of AM630 (10 mg/kg or 20 mg/kg, q.d.)…”

“…or b.i.d.) [61], OM-induced colitis (2.5 mg/kg, b.i.d.) [64], and spontaneous colitis in IL-10 À/À mice (2.5 mg/kg, q.a.d.)…”

Abstracts for 3rd French-Romanian Colloquium on Medicinal Chemistry, Iasi, Romania

“…[7][8][9] The beneficial role of CB 2 in intestinal inflammation has been highlighted in several in vivo and in vitro studies. [10][11][12][13] Moreover, the genetic invalidation of FAAH in animals with 2,4-dinitrobenzene sulfonic acid (DNBS)-induced colitis significantly reduced tissue inflammation. 14 It has also been showed that URB597, a FAAH inhibitor, increased survival and decreased inflammation in mice suffering from trinitrobenzene sulfonic acid (TNBS)-induced colitis.…”