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炎症性肠病中的肠道运动障碍:平滑肌收缩活性降低的机制

Intestinal dysmotility in inflammatory bowel disease: mechanisms of the reduced activity of smooth muscle contraction.

作者信息

Ozaki Hiroshi, Hori Masatoshi, Kinoshita Kazuya, Ohama Takashi

机构信息

Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo 113-8657, Japan.

出版信息

Inflammopharmacology. 2005;13(1-3):103-11. doi: 10.1163/156856005774423773.

Abstract

Inflammation suppresses intestinal motility, which secondarily induces abnormal growth of intestinal flora. Disturbance of this flora plays a role in the pathogenesis of mucosal inflammation, which in turn aggravates the intestinal dysmotility. Therefore, it is important to know the mechanism of alteration in motor function in the inflamed intestine. Recent studies have shown molecular mechanisms responsible for the motility disorder in the inflamed gut. These include an increase in the activity of myosin light-chain phosphatase and an alteration of ion channel activity in smooth muscle cells.

摘要

炎症会抑制肠道蠕动,进而导致肠道菌群异常生长。这种菌群紊乱在黏膜炎症的发病机制中起作用,反过来又会加重肠道动力障碍。因此,了解炎症肠道中运动功能改变的机制很重要。最近的研究揭示了炎症肠道中动力障碍的分子机制。这些机制包括肌球蛋白轻链磷酸酶活性增加和平滑肌细胞离子通道活性改变。

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