Akademik Veri Yönetim Sistemi
INTERNATIONAL SURGERY, cilt.99, sa.6, ss.757-763, 2014 (SCI-Expanded)
Hepatic ischemia reperfusion (IR) injury has complex mechanisms. We investigated the effect of dexketoprofen on endogenous leptin and malondialdehyde (MDA) levels. Wistar albino rats were divided into 4 equal groups and were subjected to 1-hour ischemia and different subsequent reperfusion intervals. Dexketoprofen was administered in a dose of 25 mg/kg 15 minutes before ischemia induction and 1-hour reperfusion to the Dexketoprofen one-hour reperfusion group, n = 6 (DIR1) group and 6-hour reperfusion to the Dexketoprofen six-hour reperfusion group, n = 6 (DIR6) group. In the control groups, 0.9% physiologic serum (SF) was administered 15 minutes before ischemia induction and 1-hour reperfusion to the one-hour reperfusion group, n = 6 (IR1) group and 6-hour reperfusion to the six-hour reperfusion group, n = 6 (IR6) group. Although serum leptin (P = 0.044) and hepatic tissue MDA levels (P = 0.004) were significantly higher in the IR6 group than in the IR1 group, there were no significant differences in dexketoprofen pretreatment between the DIR1 and DIR6 groups. There were no differences in serum MDA levels among the 4 groups, and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were significantly higher in the IR1 (P = 0.026 and P = 0.018, respectively) and IR6 (P = 0.000 and P = 0.002, respectively) groups than in the DIR1 and DIR6 groups. Dexketoprofen pretreatment can protect the liver from IR injury by decreasing inflammation and lipid peroxidation. Our study shows that dexketoprofen has no effects on endogenous leptin during IR injury.