Giakoustidis D E, Iliadis S, Tsantilas D, Papageorgiou G, Kontos N, Kostopoulou E, Botsoglou N A, Gerasimidis T, Dimitriadou A
Fifth Surgical Department, Aristotle University, Hospital Hippokration, Konstantinoupoleos 49, 54642 Thessaloniki, Greece.
Hepatogastroenterology. 2003 Sep-Oct;50(53):1587-92.
BACKGROUND/AIMS: The implication of lipid peroxidation in the inhibitory effect of GdCl3 (gadolinium chloride) on Kupffer cells activation has not been extensively investigated. The aim of this study was to examine the effect of GdCl3 inhibition of Kupffer cells activation on lipid peroxidation after severe total hepatic ischemia/reperfusion.
Male Wistar rats (n = 40) were randomly divided into a sham-operation group, a control ischemia/reperfusion group, and two ischemia/reperfusion groups pretreated with GdCl3 (10 mg and 20 mg/kg bw intravenously, 48 and 24 h prior to operation). Following 60 min of total hepatic ischemia and 120 min of reperfusion, the rats were sacrificed, and liver samples were taken for determination of malondialdehyde and light microscopy examination. Blood samples were also taken for assay of aspartate and alanine transaminase. Additional animals (n = 60) were followed up for a 7-day survival rate determination.
Ischemia/reperfusion decreased the survival rate to 13.3%, increased (p < 0.001) the levels of aspartate and alanine transaminase in serum to 2387 +/- 75 and 2157 +/- 87 IU/L, respectively, and increased (p < 0.001) malondialdehyde levels in liver to 1.609 +/- 0.096 nmoles/g compared with 1.164 +/- 0.060 in the sham operation group. Pretreatment with GdCl3 increased the survival rate to 60%, and decreased (p < 0.001) the levels of aspartate transaminase in serum to 1549 +/- 66 and 1496 +/- 55 IU/L, the levels of alanine transaminase in serum to 1302 +/- 48 and 1305 +/- 63 IU/L, and the levels of malondialdehyde in liver to 1.132 +/- 0.034 and 1.149 +/- 0.57 nmoles/g for the lower and the higher doses of GdCl3, respectively. Histological examination showed protection of liver parenchyma in the animals treated with GdCl3.
Experimental data suggest that GdCl3 inhibition of Kupffer cells activation protects liver from ischemia/reperfusion injury by a mechanism that reduces lipid peroxidation.
背景/目的：氯化钆（GdCl3）对库普弗细胞激活的抑制作用中脂质过氧化的影响尚未得到广泛研究。本研究旨在探讨严重全肝缺血/再灌注后GdCl3抑制库普弗细胞激活对脂质过氧化的影响。
将40只雄性Wistar大鼠随机分为假手术组、对照缺血/再灌注组以及两组术前用GdCl3预处理的缺血/再灌注组（分别于术前48小时和24小时静脉注射10mg/kg体重和20mg/kg体重的GdCl3）。在全肝缺血60分钟和再灌注120分钟后，处死大鼠，取肝脏样本测定丙二醛并进行光学显微镜检查。同时采集血样检测天冬氨酸转氨酶和丙氨酸转氨酶。另外选取60只动物测定7天生存率。
缺血/再灌注使生存率降至13.3%，血清中天冬氨酸转氨酶和丙氨酸转氨酶水平分别升高（p<0.001）至2387±75和2157±87IU/L，肝脏中丙二醛水平升高（p<0.001）至1.609±0.096nmol/g，而假手术组为1.164±0.060nmol/g。GdCl3预处理使生存率提高至60%，低剂量和高剂量GdCl3组血清中天冬氨酸转氨酶水平分别降至1549±66和1496±55IU/L，血清中丙氨酸转氨酶水平分别降至1302±48和1305±63IU/L，肝脏中丙二醛水平分别降至1.132±0.034和1.149±0.57nmol/g。组织学检查显示GdCl3处理的动物肝脏实质得到保护。
实验数据表明，GdCl3抑制库普弗细胞激活通过减少脂质过氧化的机制保护肝脏免受缺血/再灌注损伤。
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