Distribution of calcitonin gene-related peptide, somatostatin, substance P and vasoactive intestinal polypeptide in experimental colitis in rats

被引:0
|
作者
Miampamba, M [1 ]
Sharkey, KA [1 ]
机构
[1] Univ Calgary, Dept Phys & Biophys, Neurosci Res Grp, Calgary, AB T2N 4N1, Canada
关键词
B-50 (GAP-43); enteric nervous system; immunohistochemistry; peptides; PGP; 9.5; TNBS colitis;
D O I
暂无
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Immunohistochemistry was used to examine the distribution of calcitonin gene-related peptide (CGRP), substance P, somatostatin and vasoactive intestinal polypeptide (VIP) in experimental colitis induced with trinitrobenzene sulphonic acid (TNBS) in rats. CGRP immunoreactivity was observed throughout the colonic wall. A significant reduction of CGRP-immunoreactive (IR) nerve fibres was observed in the mucosa after the induction of colitis. After TNBS treatment substance P immunoreactivity was reduced throughout the colon; however, after 7 days there was a marked re-innervation of the circular muscle. Somatostatin immunoreactivity was distributed sparsely within the colonic wall, and was comparatively less affected by colitis. VIP immunoreactivity was abundantly distributed in the colonic wall and underwent an immediate reduction in the mucosa after TNBS treatment. After 2 days, there was a consistent and progressive increase in the number and density of VIP-IR nerve fibres in the inflamed colon, particularly the circular muscle. This change was associated with a proliferation of nerve fibres within the muscle layers. It was concluded that the early decrease in these neuropeptides was consistent with release from peripheral nerve terminals or the loss of nerves during the initial stages of colonic inflammation, which may be an essential condition for the development of colitis in this model. The observation that the intensity and density of substance P and VIP-IR nerve fibres increased in the circular muscle 7 days after the induction of colitis suggests their possible involvement in tissue repair.
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页码:315 / 329
页数:15
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