Polyethylene glycol-superoxide dismutase inhibits lipid peroxidation in hepatic ischemia/reperfusion injury.

Polyethylene glycol-superoxide dismutase inhibits lipid peroxidation in hepatic ischemia/reperfusion injury.
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DOI:
10.1186/cc358
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发表时间:
1999
期刊:
Critical care (London, England)
影响因子:
--
通讯作者:
Kirkpatrick JR
Kirkpatrick JR
中科院分区:
其他
文献类型:
--
作者:
Nguyen WD;Kim DH;Alam HB;Provido HS;Kirkpatrick JR

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缺血/再灌注后的肝损伤归因于 氧自由基(OFR)介导的脂质过氧化反应的发展 可以通过其副产品来衡量的过程,特别是 丙二醛使用自由基清除剂可以提供显著的 保护OFR诱导的肝损伤。我们假设一种新的强效 氧自由基清除剂聚乙二醇超氧化物歧化酶(PEG-SOD)能抑制 氧自由基介导的肝脏缺血/再灌注损伤中的脂质过氧化作用对12只雄性Sprague-Dawley大鼠(300-350 g)进行以下处理: 阻断肝左、肝中动脉和门静脉90 min, 再灌注120 min。PEG-SOD(5000单位/kg)静注 在血管闭塞前和再灌注后立即对6只大鼠再次进行。 其余6只大鼠给予生理盐水作为对照 组肝右叶(用作内部对照)和肝左叶 分别收获并测量组织丙二醛。生理盐水组脂质过氧化物含量明显增加 再灌注2 h组。用PEG-SOD处理阻止了组织中 丙二醛左心室与右心室之间的丙二醛平均差异 肝右叶为13.20 ± 6.35和1.70 ± 3.65nmol/g 生理盐水对照组和PEG-SOD组。该差异 发现具有统计学显著性(P < 0.005), 学生t检验。PEG-SOD能有效减轻肝脏缺血再灌注损伤 通过抑制OFR介导的脂质过氧化损伤。
Hepatic injury after ischemia/reperfusion is attributed to the development of oxygen free radical (OFR)-mediated lipid peroxidation - a process that can be measured through its byproducts, specifically malondialdehyde. The use of free radical scavengers can offer significant protection against OFR-induced liver injury. We hypothesize that a new potent OFR scavenger, polyethylene glycol-superoxide dismutase (PEG-SOD), can inhibit OFR-mediated lipid peroxidation in hepatic ischemia/reperfusion injury. Twelve male Sprague-Dawley rats (300-350 g) were subjected to occlusion of the left and middle hepatic arteries and portal veins for 90 min, followed by 120 min reperfusion. PEG-SOD (5000 units/kg) was given intravenously before vascular occlusion and again immediately upon reperfusion to six rats. Normal saline was given to the remaining six rats to be used as a control group. The right hepatic lobe (used as internal control) and left hepatic lobe were harvested separately and tissue malondialdehyde was measured. A marked increase in lipid peroxide was found in the normal saline group after 2 h reperfusion. Treatment with PEG-SOD prevented the rise in tissue malondialdehyde. The mean difference in the malondialdehyde between the left and right hepatic lobes were 13.20 ± 6.35 and 1.70 ± 3.65 nmol/g in the normal saline (control) and PEG-SOD groups, respectively. This difference was found to be statistically significant (P < 0.005) using Student's t-test. PEG-SOD can effectively attenuate hepatic ischemia/reperfusion injury by inhibiting OFR-mediated lipid peroxidation.