INVOLVEMENT OF CALCITONIN-GENE-RELATED PEPTIDE IN RAT EXPERIMENTAL COLITIS
INVOLVEMENT OF CALCITONIN-GENE-RELATED PEPTIDE IN RAT EXPERIMENTAL COLITIS
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DOI：
10.1016/0928-4257(93)90017-n
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发表时间：
1993-01-01
影响因子：
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通讯作者：
TRAMONTANA, M
中科院分区：
文献类型：
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作者：
EVANGELISTA, S;TRAMONTANA, M
本研究探讨辣椒素敏感纤维在三硝基苯磺酸(TNB)诱导的大鼠结肠炎中的作用。辣椒素(164±164momol/kgsc，2d内皮下注射)可使损伤面积和结肠湿重在攻击后24小时和1周时增加。另一方面，局部应用辣椒素(1.2-60mumol/kg)和外源性CGRP(2.6-26.3nmol/kg sc)急性刺激感觉神经可减轻TNB结肠炎的病变和减轻结肠重量的增加。在辣椒素脱敏动物中，急性辣椒素(7.7mumol/kg)的保护作用是短暂的和消失的，表明其特异性和急性释放多肽可能参与了这一机制。此外，TNB结肠炎的发生与组织中CGRP样免疫反应的选择性降低有关。这些发现提供了证据，表明辣椒素敏感神经可能通过释放保护性神经递质，如CGRP，在结肠炎中发挥防御作用。
This study investigated the role of capsaicin-sensitive fibers on trinitrobenzensulphonic acid (TNB)-induced colitis in rats. Capsaicin pretreatment (164 + 164 mumol/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 mumol/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 mumol/kg) was transient and lost in capsaicin-desensitized animals, showing its specificity and the likely participation of acute release of peptides in this mechanism. 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.