Abstract
Inflammatory bowel disease (IBD) is a general term used to describe a group of chronic inflammatory conditions of the gastrointestinal tract of unknown etiology, including two primary forms: Crohn’s disease (CD) and ulcerative colitis (UC). The endocannabinoid system (ECS) plays an important role in modulating many physiological processes including intestinal homeostasis, modulation of gastrointestinal motility, visceral sensation, or immunomodulation of inflammation in IBD. It consists of cannabinoid receptors (CB1 and CB2), transporters for cellular uptake of endocannabinoid ligands, endogenous bioactive lipids (Anandamide and 2-arachidonoylglycerol), and the enzymes responsible for their synthesis and degradation (fatty acid amide hydrolase and monoacylglycerol lipase), the manipulation of which through agonists and antagonists of the system, shows a potential therapeutic role for ECS in inflammatory bowel disease. This review summarizes the role of ECS components on intestinal inflammation, suggesting the advantages of cannabinoid-based therapies in inflammatory bowel disease.
Highlights
Inflammatory bowel disease (IBD) constitutes a group of chronic, relapsing, and incurable diseases of unknown etiology affecting the gastrointestinal (GI) tract that leads to the destruction of intestinal tissues and dramatically decreases the quality of affected patients’ life
With an in-depth understanding of the endocannabinoid system’s role, increasing evidence suggests a close relationship between gastrointestinal diseases and the endocannabinoid system homeostasis disturbances, suggesting that the ECS system may be an excellent future pharmacological target
Due to the relative paucity of preclinical evidence describing a beneficial role for the ECS in the treatment of gastrointestinal diseases in humans, the often varying and ambiguous expression levels of the ECS system compounds depending on the disease entity and the multitude of mediators associated with endocannabinoids, makes the matter quite problematic
Summary
Inflammatory bowel disease (IBD) constitutes a group of chronic, relapsing, and incurable diseases of unknown etiology affecting the gastrointestinal (GI) tract that leads to the destruction of intestinal tissues and dramatically decreases the quality of affected patients’ life. It has been suggested that due to its mediation of pro-inflammatory cytokine release and activation of gut neurons in the gastrointestinal tract in rodents, GPR55 may play an essential role in the induction of intestinal inflammation [87] which has been reported by Lin et al who showed that GPR55 is present throughout virtually all of the rat intestine and is up-regulated via LPS-induced inflammation [88] This up-regulation has been confirmed in IBD patients, where mRNA expression levels and colonic GPR55 concentrations, were significantly higher than in controls [89]. The rapidly increasing number of reported intoxication and acute failures must be taken into specific consideration and special emphasis given to further research and registration of these compounds [167]
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