中文摘要：

目的研究肝缺血再灌注（IR）损伤中蛋白合成能力下降的机制及真核生物翻译起始因子2α（eIF-2α）磷酸化的作用。方法采用大鼠肝脏瓜模型，将健康雄性SD大鼠84只随机分成2组，分别为A（缺血30min），B（缺血60min）。每组再随机分为对照组（仅解剖肝门），再灌注1，6，12，24，48，96h组。各组到预定时相检测肝组织匀浆总超氧化物歧化酶（T-SOD）、血清前白蛋白（PA）、免疫组化检测磷酸化eIF-2α，并进行统计学处理。结果T-SOD在A组中再灌注1，6，12h与对照组均有差异（P〈0．01），B组中再灌注1，6，12，24h与对照组均有差异（P〈0．01），A，B组间比较，1，6，12h均有差异（P〈0．05）；PA在各组中均在再灌注12h降至最低点，B组中各时相PA值较A组均下降，其中12，24，48h有差异（P〈0．05）；对照组肝细胞胞浆中磷酸化eIF-2α阳性表达颗粒稀少，再灌注各组阳性表达增强，A，B组间比较，1，48h均有差异（P〈0．05）；磷酸化eIF-2Q表达与PA浓度呈负相关（P〈0．01）。结论肝脏IR损伤可造成肝细胞蛋白合成能力下降；IR损伤可造成肝细胞内氧自由基过量生成，导致内质网应激，使肝细胞磷酸化eIF-2α表达增强；eIF-2α磷酸化程度增强可能是导致肝脏瓜损伤中蛋白合成能力下降的重要机制。

英文摘要：

Objective To investigate the mechanism of protein synthesis decreasing after hepatic ischemia/reperfusion injury and the role of phosphorylated eukaryotie initiation faetor 2α （eIF-2α）. Methods Eighty-four healthy male SD rats were randomized into 2 groups. The isehemia lasted for 30 min and 60 min in group A and B, respectively. The rats in eaeh group were further divided into the control and 6 subgroups corresponding to 1, 6, 12, 24, 48 and 96h after reperfusion. The levels of TSOD and prealhumin （PA） were determined in all the groups. The phosphorylated eIF-2α was detected with immunohistochemistry. Results There were signifieant differences between the control group and subgroups corresponding to 1, 6 and 12 h after liver reperfusion in group A and group B （P〈 0. 01）. At 1, 6 and 12 h after liver reperfusion, the level of T-SOD was markedly lower in group A than in group B （P〈0.05）. The serum concentration of PA was the lowest at 12 h after reperfusion in both groups and there were significant differences in subgroups corresponding to 12, 24 and 48h after reperfusion between group A and group B. The inereased expression of phosphorylated eIF-2α was remarkably higher in group B than in group A （P〈0. 05）. The negative correlation of phosphorylated eIF-2α to PA existed in the liver （P〈0. 01）. Conclusions The ability of protein synthesis was significantly decreased during hepatie isehemia/reperfusion. Meanwhile, the oxygen-derived free radicals are excessively produced, whieh makes endoplasmie retieulum stress and provoke eIF-2α kinase to increase the expression of phosphorylated eIF-2α. The increased expression of phosphorylated eIF-2α might be the important mechanism of low ability of protein synthesis.