Involvement of calcitonin gene-related peptide in rat experimental colitis

https://doi.org/10.1016/0928-4257(93)90017-NGet rights and content

Abstract

This study investigated the role of capsaicin-sensitive fibers on trinitrobenzensulphonic acid (TNB)-induced colitis in rats. Capsaicin pretreatment (164 + 164 μmol/kg sc in 2 days) produced an increase of damaged area and colon wet weight at 24 h and 1 week after the challenge. On the other hand, acute stimulation of sensory nerves by local application of capsaicin (1.2–60 μmol/kg) as well as exogenous administration of CGRP (2.6–26.3 nmol/kg sc) ameliorated the lesions and reduced the increase of colon weight in TNB-colitis. The protective effect of acute capsaicin (7.7 μmol/kg) was transient and lost in capsaicin-desensitized animals, showing its specificity and the likely participation of acute release of peptides in this mechanisms. Moreover, development of TNB colitis was associated with a selective decrease in tissue CGRP-like immunoreactivity. These findings provide evidence that capsaicin-sensitive nerves, probably via the release of protective neurotransmitters such as CGRP, play a defensive role in colitis.

References (19)

There are more references available in the full text version of this article.

Cited by (29)

  • Opposite effects of substance P and calcitonin gene-related peptide in oxazolone colitis

    2012, Digestive and Liver Disease
    Citation Excerpt :

    NK-1 blockers were also beneficial in a T cell transfer model of chronic colitis [8]. A protective role of CGRP in colitis has been suggested by several pharmacological studies on TNBS colitis in rats [5,7,33]. In addition, knockdown by double-stranded RNA against the calcitonin receptor-like receptor for CGRP resulted in a significantly greater degree of oedema and necrosis than in sham-treated rats in TNBS colitis [34].

  • TRPA1 and substance P mediate colitis in mice

    2011, Gastroenterology
    Citation Excerpt :

    In contrast, another neurokinin1 antagonist was ineffective in rat TNBS colitis.19,22 An opposite, protective, role of CGRP was suggested by several pharmacologic studies on rat TNBS colitis.20,22,71 In addition, knockdown by double-stranded RNA against the calcitonin receptor-like receptor for CGRP resulted in a significantly greater degree of edema and necrosis than in sham-treated rats with TNBS colitis.72

View all citing articles on Scopus
View full text