胃黏膜血流力学特性对胃黏膜损伤的作用及机制研究

Gastric mucosal blood flow is an important part of gastric mucosal defense and repair mechanisms. The reduction of gastric mucosal blood flow is central to the occurrence of gastric mucosal injury. Glucagon like peptide -2 (GLP-2) is a protective factor of the gastrointestinal tract, and its target organ is limited to the gastrointestinal tract. Recent studies have found that GLP-2 has a role in increasing gastrointestinal blood flow, but the mechanism is not clear. This study is based on the animal model of gastric mucosal injury induced by ethanol, combined with animal experiments and the measurement of hemodynamic characteristics, to study biomechanical and biological effects of GLP-2 on gastric mucosal vascular. We will explore that CGPR, NO pathway and endogenous prostaglandins may be involved in GLP-2 by increasing the blood flow on gastric mucosa repair(protection) effect of gastric mucosal injury induced by ethanol and GLP-2, hemodynamic characteristics, CGPR, NO pathway and endogenous prostaglandins in mechanism and biological effect of gastric mucosal injury and repair. The results will contribute to understanding of the mechanism of gastric mucosal injury, the mechanism of gastric mucosal repair and efficiency of GLP-2. It will be helpful to search for new drug targets. It has important significance for prevention and treatment of gastric mucosal injury.

胃黏膜血流是胃黏膜防御-修复机制的重要组成部分，胃黏膜血流下降是胃黏膜损伤发生的中心环节。胰高血糖素样肽-2 （GLP-2）是胃肠道的保护性因子，其作用靶器官仅限于胃肠道，近来研究发现GLP-2有增加胃肠道血流的作用，但机理尚不清楚。本研究基于乙醇诱导的胃黏膜损伤动物模型，结合动物实验和血流力学特性测量，研究GLP-2等作用下胃黏膜血管的生物力学与生物学效应；探讨CGPR、NO通路和内源性前列腺素可能参与了GLP-2通过增加胃黏膜血流对乙醇诱导的胃黏膜损伤的修复（保护）作用，探索GLP-2、血流力学特性、CGPR、NO通路与内源性前列腺素在胃黏膜损伤与修复的作用机制和生物学效应。结果将有助于更好地了解胃黏膜损伤机制，理解GLP-2对胃黏膜损伤修复的机理与效能，这对寻找新的药物作用靶点、对胃黏膜损伤的防治具有重要意义。