Tryptase and Protease-Activated Receptor 2 Expression Levels in Irritable Bowel Syndrome

肠易激综合征中的类胰蛋白酶和蛋白酶激活受体 2 的表达水平

阅读:6
作者:Wen-Jing Liang, Guo Zhang, He-Sheng Luo, Lie-Xin Liang, Dan Huang, Fa-Can Zhang

Aims

Previous studies have revealed that mast cells (MCs) may activate the protease-activated receptors and release of neuropeptides involved in the pathogenesis of irritable bowel syndrome (IBS). The levels of proteaseactivated receptor 2 (PAR-2) and tryptase can contribute to understanding the pathogenesis of IBS.

Background/aims

Previous studies have revealed that mast cells (MCs) may activate the protease-activated receptors and release of neuropeptides involved in the pathogenesis of irritable bowel syndrome (IBS). The levels of proteaseactivated receptor 2 (PAR-2) and tryptase can contribute to understanding the pathogenesis of IBS.

Conclusions

Tryptase levels may upregulate the function of PAR- 2, resulting in the release of neuropeptide and they were correlated with clinical symptoms associated with IBS.

Methods

Colonoscopic biopsies were performed of 38 subjects (20 with IBSdiarrhea [IBS-D], eight with IBS-constipation [IBS-C], and 10 healthy volunteers). The mRNA and protein levels of tryptase and PAR-2 were assessed by real-time PCR and Western blot. The levels of vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) were measured by immunohistochemistry, and MCs were counted by toluidine blue staining.

Results

Significant increases in the mRNA expression of tryptase (p<0.05, IBS-D, IBS-C vs control) and PAR-2 (p<0.05, IBS-D, IBS-C vs control) and in the tryptase protein level (p<0.05, IBS-D, IBS-C vs control) were detected in IBS. Elevations of MCs, CGRP, VIP and SP (p<0.05, IBS-D vs control) were observed for IBS-D only. Conclusions: Tryptase levels may upregulate the function of PAR- 2, resulting in the release of neuropeptide and they were correlated with clinical symptoms associated with IBS.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。