Endocannabinoid overactivity and intestinal inflammation
Endocannabinoid overactivity and intestinal inflammation
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DOI：
10.1136/gut.2005.090472
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发表时间：
2006-10-01
期刊：
影响因子：
24.5
通讯作者：
Izzo, A. A.
中科院分区：
文献类型：
--
作者：
Di Marzo, V.;Izzo, A. A.
大麻素受体1型和2型（CB 1和CB 2），内源性配体，激活他们（内源性大麻素），内源性大麻素的生物合成和失活的机制已被确定在胃肠道系统。内源性大麻素激活CB 1受体可松弛食管下括约肌，抑制胃酸分泌、肠蠕动和液体刺激分泌。然而，大麻素受体的刺激以其他几种方式影响胃肠道功能。最近的数据表明，在动物模型和人类炎症性疾病的炎症过程中，小肠和结肠中的内源性大麻素系统被过度刺激。这种“内源性大麻素过度活跃”的病理意义及其可能用于治疗目的的开发在这里进行了讨论。
Cannabinoid receptors of type 1 and 2 (CB1and CB2), endogenous ligands that activate them (endocannabinoids), and mechanisms for endocannabinoid biosynthesis and inactivation have been identified in the gastrointestinal system. Activation of CB1receptors 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.