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右酮洛芬对肝脏缺血再灌注损伤期间内源性瘦素和脂质过氧化的影响。

The effects of dexketoprofen on endogenous leptin and lipid peroxidation during liver ischemia reperfusion injury.

作者信息

Ustun Yasemin Burcu, Koksal Ersin, Kaya Cengiz, Sener Elif Bengi, Aksoy Abdurrahman, Yarim Gul, Kabak Yonca, Gulbahar Yavuz

机构信息

1 Department of Anesthesiology and Reanimation, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

出版信息

Int Surg. 2014 Nov-Dec;99(6):757-63. doi: 10.9738/INTSURG-D-14-00121.1.

Abstract

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.

摘要

肝缺血再灌注(IR)损伤机制复杂。我们研究了右酮洛芬对内源性瘦素和丙二醛(MDA)水平的影响。将Wistar白化大鼠分为4组,每组数量相等,进行1小时的缺血及不同时长的后续再灌注。在缺血诱导前15分钟和再灌注1小时给右酮洛芬1小时再灌注组(n = 6,DIR1组)给予25 mg/kg剂量的右酮洛芬,给右酮洛芬6小时再灌注组(n = 6,DIR6组)在缺血诱导前15分钟和再灌注6小时给予该剂量药物。在对照组中,在缺血诱导前15分钟和再灌注1小时给1小时再灌注组(n = 6,IR1组)给予0.9%生理血清(SF),给6小时再灌注组(n = 6,IR6组)在缺血诱导前15分钟和再灌注6小时给予该血清。尽管IR6组血清瘦素(P = 0.044)和肝组织MDA水平(P = 0.004)显著高于IR1组,但DIR1组和DIR6组在右酮洛芬预处理方面无显著差异。4组间血清MDA水平无差异,IR1组(分别为P = 0.026和P = 0.018)和IR6组(分别为P = 0.000和P = 0.002)的血清天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)活性显著高于DIR1组和DIR6组。右酮洛芬预处理可通过减轻炎症和脂质过氧化保护肝脏免受IR损伤。我们的研究表明,右酮洛芬在IR损伤期间对内源性瘦素无影响。

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