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神经递质、肠道激素及炎症介质对大鼠结肠黏液分泌的影响。

Effects of neurotransmitters, gut hormones, and inflammatory mediators on mucus discharge in rat colon.

作者信息

Plaisancié P, Barcelo A, Moro F, Claustre J, Chayvialle J A, Cuber J C

机构信息

Institut National de la Santé et de la Recherche Médicale U-45, Hôpital Edouard Herriot, 69347 Lyon Cedex 03, France.

出版信息

Am J Physiol. 1998 Nov;275(5):G1073-84. doi: 10.1152/ajpgi.1998.275.5.G1073.

DOI:10.1152/ajpgi.1998.275.5.G1073
PMID:9815038
Abstract

The effect of potential mediators of mucus secretion was investigated in the isolated vascularly perfused rat colon by using a sandwich enzyme-linked immunosorbent assay for rat colonic mucin and by histochemical analysis. Bethanechol (100-200 microM), bombesin (100 nM), and vasoactive intestinal peptide (VIP, 100 nM) provoked a dramatic mucin discharge (maximal response at 900, 900, and 600% of control loops, respectively). VIP-stimulated mucin secretion was abolished by tetrodotoxin, whereas atropine was without effect. In contrast, both tetrodotoxin and atropine significantly decreased mucin release induced by bombesin. Isoproterenol or calcitonin gene-related peptide was without effect. Serotonin (1-5 microM) and peptide YY (10 nM) evoked mucin discharge, whereas glucagon-like peptide-1 did not release mucin. Finally, bromolasalocid (20 microM), interleukin-1beta (0.25 nM), sodium nitroprusside (1 mM), and dimethyl-PGE2 (2.5 microM) induced mucus discharge. The results demonstrated a good correlation between the immunological method and histological analysis. In conclusion, these findings suggest a role for the enteric nervous system, the enteroendocrine cells, and resident immune cells in mediation of colonic mucus release.

摘要

通过使用大鼠结肠粘蛋白夹心酶联免疫吸附测定法和组织化学分析,在离体血管灌注大鼠结肠中研究了粘液分泌潜在介质的作用。氨甲酰甲胆碱(100 - 200微摩尔)、蛙皮素(100纳摩尔)和血管活性肠肽(VIP,100纳摩尔)引起了显著的粘蛋白释放(分别在对照肠袢的900%、900%和600%时达到最大反应)。河豚毒素消除了VIP刺激的粘蛋白分泌,而阿托品则无作用。相比之下,河豚毒素和阿托品均显著降低了蛙皮素诱导的粘蛋白释放。异丙肾上腺素或降钙素基因相关肽无作用。血清素(1 - 5微摩尔)和肽YY(10纳摩尔)引起粘蛋白释放,而胰高血糖素样肽-1不释放粘蛋白。最后,溴氯杀鼠灵(20微摩尔)、白细胞介素-1β(0.25纳摩尔)、硝普钠(1毫摩尔)和二甲基前列腺素E2(2.5微摩尔)诱导粘液释放。结果表明免疫方法与组织学分析之间具有良好的相关性。总之,这些发现提示肠神经系统、肠内分泌细胞和驻留免疫细胞在结肠粘液释放的介导中起作用。

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