Cannabinoids in intestinal inflammation and cancer

Izzo, Angelo A.; Camilleri, Michael

doi:10.1016/j.phrs.2009.03.008

Cited by 91 publications

(72 citation statements)

References 114 publications

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“…A recent article has highlighted that between 33 and 50% of people suffering from IBD have been using Cannabis to relieve IBD-related symptoms [4] . In line with this, animal models of IBD largely suggest that cannabinoid compounds and activation of cannabinoid (CB) receptors significantly suppress the severity of colitis [5][6][7] . In addition, non-CB receptormediated effects of cannabinoids can also cause improvement of experimental colitis [8,9] .…”

Section: Introductionmentioning

confidence: 87%

Topical and Systemic Cannabidiol Improves Trinitrobenzene Sulfonic Acid Colitis in Mice

Schicho

Storr

2012

Pharmacology

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Section: Introductionmentioning

confidence: 87%

Topical and Systemic Cannabidiol Improves Trinitrobenzene Sulfonic Acid Colitis in Mice

Schicho

Storr

2012

Pharmacology

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“…In brief, cells were seeded onto the upper side of the transwell inserts in serum-free DMEM and immediately treated with test substances or vehicles for the indicated times. DMEM (high glucose, GlutaMAX™) containing 10% (v/v) FCS (22)(23)(24)(25). As a consequence of these fi ndings, cannabinoids have gained interest as potential options for the treatment of osteodegenerative disorders such as osteoporosis ( 24,(26)(27)(28) or neurodegenerative diseases such as Parkinson's disease ( 29 ).…”

Section: Migration Assaymentioning

confidence: 99%

Inhibition of FAAH confers increased stem cell migration via PPARα

Wollank

Ramer

Ivanov

et al. 2015

Journal of Lipid Research

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review see ( 1 )]. As a consequence, components of this system, as well as pharmacological strategies to block endocannabinoid degradation, have been elucidated in past years [for review see ( 2 )].An integral component of the endocannabinoid system is the enzyme, fatty acid amide hydrolase (FAAH), a serine hydrolase fi rst identifi ed as the principal catabolic enzyme of the endocannabinoid, anandamide [ N -arachidonoylethanolamine (AEA)] ( 3 ). The second major endocannnabinoid, 2-arachidonoylglycerol (2-AG), can be hydrolyzed by multiple enzymes, including FAAH and monoacylglycerol lipase (MAGL), with about 85% of brain 2-AG hydrolase activity ascribed to MAGL ( 4 ). Likewise, FAAH is the catabolic enzyme for the endocannabinoid-like substances, Noleoylethanolamine (OEA) and N -palmitoylethanolamine (PEA) ( 5 ). In contrast to AEA and 2-AG, both endocannabinoid-like substances do not bind to the cannabinoid receptors, CB 1 and CB 2 , but share an activation of the nonselective cation channel transient receptor potential vanilloid 1 (TRPV1) ( 6-9 ) and the transcription factor PPAR ␣ ( 10-16 ) with endocannabinoids. In line with the latter notion, various biological effects of FAAH inhibitors have been associated with activation of PPAR ␣ ( 17-21 ).Several components of the endocannabinoid system, including CB 1 , CB 2 , TRPV1, and cannabinoid receptor ligands, have been reported as effectors of tissue healing

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“…In addition, evidence is emerging that exogenous and endogenous CBs have an important role in GI physiopathology, such as GI inflammation [16]. Figure 1 summarizes the main effects induced by CBs in the GI tract.…”

Section: The Endocannabinoid System In the Gastrointestinal Tractmentioning

confidence: 99%

“…In these models, both CB1 and CB2 receptor activation may reduce hypermotility associated with gut inflammation and/or immune activation, as well as decreasing pain, intestinal fluid volume and inflammation (review in Izzo and Sharkey [11] and Izzo and Camilleri [16]). A beneficial effect has been shown for THC, CB1 and CB2 agonists and inhibitors of anandamide or 2-AG degradation/reuptake [11,16,67]. Activation of not only CB1 [68], but also CB2 receptors [14] reduced electrically evoked contractions of muscle preparations from inflamed gut.…”

Section: Cb Effects On Altered Gi Motilitymentioning

confidence: 99%

The Gastrointestinal Pharmacology of Cannabinoids: Focus on Motility

et al. 2012

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The marijuana plant Cannabis sp. and its derivatives and analogues, known as cannabinoids (CBs), induce many effects throughout the whole body. Herein we briefly review the gastrointestinal (GI) pharmacology of CBs, with special focus on motor function. Some drugs are available to treat nausea and emesis, and evidences in humans and animal models suggest that other GI motility alterations (gastro-oesophageal reflux, inflammatory bowel conditions or paralytic ileus) might benefit from modifications of the CB tone throughout the gut. However, central and peripheral (including GI) side effects may occur upon acute and chronic CB administration. Hopefully, the ongoing worldwide intense research on CBs will soon provide new, safer CB-based medicines.

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Cannabinoids in intestinal inflammation and cancer

Cited by 91 publications

References 114 publications

Topical and Systemic Cannabidiol Improves Trinitrobenzene Sulfonic Acid Colitis in Mice

Topical and Systemic Cannabidiol Improves Trinitrobenzene Sulfonic Acid Colitis in Mice

Inhibition of FAAH confers increased stem cell migration via PPARα

The Gastrointestinal Pharmacology of Cannabinoids: Focus on Motility

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