Di Marzo V, Izzo A A
Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, via Campi Flegrei 34, 80078 Pozzuoli, Napoli, Italy.
Gut. 2006 Oct;55(10):1373-6. doi: 10.1136/gut.2005.090472.
Cannabinoid receptors of type 1 and 2 (CB(1) and CB(2)), endogenous ligands that activate them (endocannabinoids), and mechanisms for endocannabinoid biosynthesis and inactivation have been identified in the gastrointestinal system. Activation of CB(1 )receptors by endocannabinoids produces relaxation of the lower oesophageal sphincter and inhibition of gastric acid secretion, intestinal motility, and fluid stimulated secretion. However, stimulation of cannabinoid receptors impacts on gastrointestinal functions in several other ways. Recent data indicate that the endocannabinoid system in the small intestine and colon becomes over stimulated during inflammation in both animal models and human inflammatory disorders. The pathological significance of this "endocannabinoid overactivity" and its possible exploitation for therapeutic purposes are discussed here.
1型和2型大麻素受体（CB(1)和CB(2)）、激活它们的内源性配体（内源性大麻素）以及内源性大麻素生物合成和失活的机制已在胃肠系统中得到确认。内源性大麻素对CB(1)受体的激活会导致食管下括约肌松弛，并抑制胃酸分泌、肠道蠕动以及液体刺激分泌。然而，大麻素受体的刺激还会通过其他几种方式影响胃肠功能。最近的数据表明，在动物模型和人类炎症性疾病中，小肠和结肠中的内源性大麻素系统在炎症期间会受到过度刺激。本文将讨论这种“内源性大麻素活性过高”的病理意义及其在治疗方面的潜在应用。
