Eysselein V E, Reinshagen M, Patel A, Davis W, Nast C, Sternini C
Inflammatory Bowel Disease Center, Harbor-UCLA Medical Center, Torrance 90509.
Ann N Y Acad Sci. 1992 Jun 30;657:319-27. doi: 10.1111/j.1749-6632.1992.tb22779.x.
Pronounced changes in gut neuropeptide content have been observed in colonic tissues from animals with acute experimental colitis and in some patients with inflammatory bowel disease. The early decrease of CGRP in the colon during colitis in the animal studies suggest that CGRP is released during the inflammatory process. No data are available showing the biological action of released CGRP during inflammation. The sensory neurotoxin capsaicin was used in animal studies to examine the effect of sensory nerves on inflammation and healing in experimental animal models. The severity of colitis was enhanced after capsaicin pretreatment in acute and chronic animal models of colitis. These data support the hypothesis that sensory nerves exert a protective and healing-promoting function in the gut. CGRP is a good candidate for this action of sensory nerves because it is a major component in sensory nerve fibers. How CGRP exerts its protective function in the intestine is unknown. Data from gastric ulcer models support the hypothesis that a main action of CGRP is regulation of mesenteric and mucosal blood flow resulting in enhanced protection and tissue healing. Other effector roles of CGRP afferent nerve endings could also be considered.
在患有急性实验性结肠炎的动物以及一些炎症性肠病患者的结肠组织中，已观察到肠道神经肽含量有明显变化。动物研究中结肠炎期间结肠中降钙素基因相关肽（CGRP）的早期减少表明CGRP在炎症过程中被释放。目前尚无数据表明炎症期间释放的CGRP的生物学作用。在动物研究中，使用感觉神经毒素辣椒素来研究感觉神经对实验动物模型中炎症和愈合的影响。在急性和慢性结肠炎动物模型中，辣椒素预处理后结肠炎的严重程度增强。这些数据支持了感觉神经在肠道中发挥保护和促进愈合功能的假说。CGRP是感觉神经这一作用的良好候选者，因为它是感觉神经纤维中的主要成分。CGRP如何在肠道中发挥其保护功能尚不清楚。来自胃溃疡模型的数据支持了这样的假说，即CGRP的主要作用是调节肠系膜和黏膜血流，从而增强保护和组织愈合。CGRP传入神经末梢的其他效应作用也可以考虑。
