کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3337802 1213817 2011 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Protective effects of glutamine preconditioning on ischemia-reperfusion injury in rats
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کبدشناسی
پیش نمایش صفحه اول مقاله
Protective effects of glutamine preconditioning on ischemia-reperfusion injury in rats
چکیده انگلیسی

BackgroundHepatic ischemia-reperfusion injury is a common phenomenon in hepatic surgical procedures and can resuit in further severe damage. This study aimed to investigate the protective effects of glutamine preconditioning on hepatic ischemia-reperfusion injury in rats and its dose-dependencyMethodsThirty-two healthy maie Wistar rats were randomly divided into four groups (n=8 per group). One group received 0.9% NaCl (control) and the other three received glutamine (Gin groups) 4 hours before ischemia. The Gin groups were named GL, GM, and GH according to the glutamine dose. The liver was subjected to 1 hour of ischemia and 2 hours of reperfusion. Two hours later, the levels of alanine aminotransferase (ALT), intracellular free calcium (Ca2+), and activity of NaVK* adenosine triphosphatase (ATPase) and Superoxide dismutase (SOD) were assessed, and liver tissue sections were examined under a microscope.ResultsThe Gin and control groups differed in the concentration of intracellular free calcium (p<0.05), and the activity of Na+/K+ ATPase and SOD in the Gin groups was higher than in the control group (p<0.05). The ALT level was lower in the GM and GH groups than in the control group (p<0.05). The levels of Na+/K+ ATPase and SOD rose gradually with increasing glutamine dose (p<0.05), and the concentration of Ca+ declined gradually with increasing glutamine dose (p<0.05). The degree of hepatocyte injury was milder in the Gin groups than in the control group.ConclusionsGlutamine preconditioning protectedeffectively against hepatic ischemia-reperfusion injury. These protective effects were related to the dose of glutamine and due to the reduction of intracellular calcium overload and the improvements in the activity of Na+/K+ ATPase and SOD.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Hepatobiliary & Pancreatic Diseases International - Volume 10, Issue 1, February 2011, Pages 78-82