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首页> 外文期刊>American Journal of Physiology >Attenuation of acute experimental colitis by preventing NPY Y1 receptor signaling.
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Attenuation of acute experimental colitis by preventing NPY Y1 receptor signaling.

机译：通过预防NPY Y1受体信号转导减轻急性实验性结肠炎。

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摘要

Neuropeptide Y (NPY), a 36-amino acid peptide, is widely expressed in the central and peripheral nervous system. NPY is involved in the regulation of several physiological processes, including energy balance, food intake, and nociception. Recently, we showed that activation of the NPY Y1 receptor is required for cutaneous neurogenic inflammation. Because neurogenic inflammation could participate in colitis, the aim of this study was to investigate the role of the NPY Y1 receptor in acute colitis using mice genetically deficient of NPY Y1 receptor. In addition, the Y1 receptor antagonist H409/22, was also investigated. Animals received 5% dextran sulfate sodium (DSS) in drinking water for 7 days. One group of animals also received the Y1 receptor antagonist, administered intraperitoneally twice daily. Disease activity was assessed daily for 7 days in all groups. DSS induced colitis in all animals resulting in weight loss, diarrhea, epithelial damage, crypt shortening, and inflammatory infiltration. However, clinical manifestation of the disease was markedly attenuated in Y1 null mutant mice as well as in mice receiving the Y1 antagonist. Histological analysis showed that tissue damage and ulceration were less severe in Y1-deficient animals. Consistent with the clinical and histological data, capsaicin-induced plasma extravasation was significantly reduced in the gut of Y1 null mutant animals compared with treated wild-type animals. These data indicate that NPY and Y1 receptor are involved in intestinal inflammation and suggest that inhibition of NPY Y1 receptor signaling may provide a novel therapeutic approach in the treatment of colonic inflammation.
机译：神经肽Y（NPY）是一种36个氨基酸的肽，在中枢神经系统和周围神经系统中广泛表达。 NPY参与多种生理过程的调节，包括能量平衡，食物摄入和伤害感受。最近，我们表明皮肤神经性炎症需要激活NPY Y1受体。由于神经性炎症可能参与结肠炎，因此本研究的目的是使用遗传上缺乏NPY Y1受体的小鼠研究NPY Y1受体在急性结肠炎中的作用。另外，还研究了Y1受体拮抗剂H409 / 22。动物在饮用水中接受5％硫酸葡聚糖硫酸钠（DSS），持续7天。一组动物还接受了每天两次腹膜内施用的Y1受体拮抗剂。在所有组中每天评估疾病活动7天。 DSS在所有动物中诱发结肠炎，导致体重减轻，腹泻，上皮损伤，隐窝缩短和炎性浸润。然而，该疾病的临床表现在Y1无效突变小鼠以及接受Y1拮抗剂的小鼠中明显减弱。组织学分析表明，Y1缺乏动物的组织损伤和溃疡程度较轻。与临床和组织学数据一致，与经治疗的野生型动物相比，Y1无效突变动物的肠道中辣椒素诱导的血浆外渗明显减少。这些数据表明NPY和Y1受体参与肠道炎症，并表明抑制NPY Y1受体信号传导可能为结肠炎的治疗提供一种新颖的治疗方法。

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