Evangelista S, Maggi M, Renzetti A R
Pharmacology Department, Istituto Farmacobiologico Malesci S.p.A., Firenze, Italy.
Neuropeptides. 1996 Oct;30(5):425-8. doi: 10.1016/s0143-4179(96)90004-9.
Neurochemical and functional studies were performed to investigate the role of substance P (SP) during trinitrobenzene sulfonic acid (TNB)-induced colitis. Time course studies showed that tissutal SP-like immunoreactivity levels decreased in acute or chronic phases of the experimental colitis. The affinity of SP was not significantly reduced up to 1 week after TNB-induced colitis but a decreased density of SP binding sites was observed at all times. The subcutaneous administration of neurokinin (NK)1 receptor antagonist RP 67580 (0.1-1 mumol/kg daily x 1 week) did not affect the injury induced by the hapten. These findings suggest that changes in SP seem to be the effect rather than the cause of colitis and differ from those observed in human inflammatory bowel diseases.
进行了神经化学和功能研究，以探讨P物质（SP）在三硝基苯磺酸（TNB）诱导的结肠炎中的作用。时间进程研究表明，在实验性结肠炎的急性期或慢性期，组织中SP样免疫反应水平降低。在TNB诱导的结肠炎后长达1周内，SP的亲和力没有显著降低，但在所有时间点均观察到SP结合位点密度降低。皮下注射神经激肽（NK）1受体拮抗剂RP 67580（0.1 - 1 μmol/kg每日×1周）不影响半抗原诱导的损伤。这些发现表明，SP的变化似乎是结肠炎的结果而非原因，并且与人类炎症性肠病中观察到的情况不同。
