摘要
Glucagon-like peptide-2 （GLP-2） has potent anti-inflammatory effects and protects against experimental ischemia/reperfusion （I/R） injury in pulmonary, intestinal, and myocardial tissue. However, its protective abilities against I/R injury in the liver are unknown. We investigated the potential role of GLP-2 pretreatment on hepatic I/R injury in rats. A total of 24 rats were randomly divided into three groups （n = 8）. The first group was the control group; the second group was the vehicle-treated hepatic ischemia/reperfusion （HIR, vehicle saline-treated） group; and the third group was the GLP-2 pretreated I/R （GLP2-IR） group. Each rat in the third group was intraperitoneally administered 5 ~tg GLP-2 for 5 d before the procedure. A portal triad was created to induce ischemia with a vascular atraumatic clamp. After 40 min, the clamp was released to initiate hepatic reperfusion for 6 h. Blood samples and tissue specimens from the fiver were obtained. Alanine aminotransferase, aspartate aminotransferase, and total bilirubin levels significantly increased in the saline- treated HIR group （P 〈 0.001）, whereas GLP-2 pretreatment significantly decreased their levels （P 〈 0.01）. Our data suggested that GLP-2 pretreatment may have a protective effect on liver I/R injury. However, dose-response studies are necessary to determine the most effective dose.
Glucagon-like peptide-2 （GLP-2） has potent anti-inflammatory effects and protects against experimental ischemia/reperfusion （I/R） injury in pulmonary, intestinal, and myocardial tissue. However, its protective abilities against I/R injury in the liver are unknown. We investigated the potential role of GLP-2 pretreatment on hepatic I/R injury in rats. A total of 24 rats were randomly divided into three groups （n = 8）. The first group was the control group; the second group was the vehicle-treated hepatic ischemia/reperfusion （HIR, vehicle saline-treated） group; and the third group was the GLP-2 pretreated I/R （GLP2-IR） group. Each rat in the third group was intraperitoneally administered 5 ~tg GLP-2 for 5 d before the procedure. A portal triad was created to induce ischemia with a vascular atraumatic clamp. After 40 min, the clamp was released to initiate hepatic reperfusion for 6 h. Blood samples and tissue specimens from the fiver were obtained. Alanine aminotransferase, aspartate aminotransferase, and total bilirubin levels significantly increased in the saline- treated HIR group （P 〈 0.001）, whereas GLP-2 pretreatment significantly decreased their levels （P 〈 0.01）. Our data suggested that GLP-2 pretreatment may have a protective effect on liver I/R injury. However, dose-response studies are necessary to determine the most effective dose.
