Department of Gastroenterology, Affiliated Hospital of Luzhou Medical College, Luzhou City, PR China.
Pancreas. 2012 Oct;41(7):1080-5. doi: 10.1097/MPA.0b013e31824966b0.
To investigate the protective effect of glucagon-like peptide 2 (GLP-2) on intestinal barrier dysfunction in severe acute pancreatitis and to explore the putative mechanism of this effect.
Thirty rats were randomly divided into 3 groups. Group 1 received sham operation. Severe acute pancreatitis was induced in group 2 and group 3 via retrograde injection of 3% sodium taurocholate to the pancreatic duct. Rats in group 3 were peritoneally injected with GLP-2. Intestinal barrier dysfunction was characterized by the histological measurements and concentration of plasma diamine oxidase. The tissue sections of ileum were collected for the detection of proliferating cell nuclear antigen protein and apoptosis.
Glucagon-like peptide 2 administration improved the ileal mucosal injury, which was also demonstrated by the histological score of ileal mucosa. The concentration of diamine oxidase was decreased in rats with acute pancreatitis treated with GLP-2. Acute pancreatitis-induced epithelial cell apoptosis was partly prevented by GLP-2. Immunohistochemical staining of proliferating cell nuclear antigen protein was increased in group 3 compared with that in group 2.
Results from this study suggest that GLP-2 has a protective effect on intestinal barrier dysfunction in rats with severe acute pancreatitis via mechanisms closely involving promotion of cell growth and inhibition of intestinal epithelial cell apoptosis.
研究胰高血糖素样肽 2（GLP-2）对重症急性胰腺炎肠屏障功能障碍的保护作用，并探讨其作用机制。
30 只大鼠随机分为 3 组。第 1 组接受假手术。第 2 组和第 3 组通过逆行胰胆管注射 3%牛磺胆酸钠诱导重症急性胰腺炎。第 3 组大鼠腹腔内注射 GLP-2。肠屏障功能障碍通过组织学测量和血浆二胺氧化酶浓度来评估。收集回肠组织切片，检测增殖细胞核抗原蛋白和细胞凋亡。
GLP-2 给药改善了回肠黏膜损伤，这也可以通过回肠黏膜的组织学评分来证明。GLP-2 治疗的急性胰腺炎大鼠二胺氧化酶浓度降低。GLP-2 部分预防了急性胰腺炎诱导的上皮细胞凋亡。与第 2 组相比，第 3 组的增殖细胞核抗原蛋白免疫组化染色增加。
本研究结果表明，GLP-2 通过促进细胞生长和抑制肠上皮细胞凋亡的机制，对重症急性胰腺炎大鼠的肠屏障功能障碍具有保护作用。
