中文摘要：

目的探讨高迁移率族蛋白B1（HMGB1）在大鼠肝脏热缺血／再灌注（I／R）损伤中的作用。方法90只Wistar大鼠被随机分为正常对照组、林格液组、丙酮酸乙酯（EP）治疗组。采用夹闭左、右肝蒂使95％肝脏缺血90min再恢复血流并切除未缺血的尾叶肝脏制模。林格液组和EP治疗组制模前分别经阴茎背静脉注射林格液4ml或EP3．26g／L（溶于林格液4ml中），于术后2、8、24、48h取下腔静脉血检测血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）水平，处死动物后检测肝组织HMGB1、肿瘤坏死因子-α（TNF—α）、白细胞介素-10（IL-10）含量。结果林格液组和EP治疗组血清ALT、AST水平均显著高于正常对照组，EP治疗组各时间点ALT及术后2h、8hAST水平均显著低于林格液组（P〈0．05或P〈0．01）。林格液组8、24、48h肝组织HMGB1水平显著高于正常对照组，EP治疗组仅48h显著升高；EP治疗组在8h、24h时HMGB1水平显著低于林格液组；林格液组和EP治疗组在8h时TNF—α水平均高于正常对照组，而EP治疗组显著低于林格液组（P〈0．05或P〈0．01）。各组IL-10水平无明显差异。结论HMGB1参与了肝I／R损伤的病理过程。

英文摘要：

Objective To investigate the potential role of high mobility group box-1 protein （HMGB1） in rats with liver warm isehemia/reperfusion （I/R） injury. Methods Ninety Wistar rats were randomly divided into three groups： normal controls （group A）, Ringer＇s solution treatment group （group B）, and Ringer＇s ethyl pyruvate （EP） treatment group （group C）. The animal model of I/R was prepared by clamping all the liver pedicles of liver lobes except caudate lobe for 90 minutes, then the un-ischemic caudate lobe was resected after liver reperfusion. The model made this way could establish 95% of liver ischemia. Just before the model establishment, the animals in group B were given 4 ml Ringer＇s solution and in group C, Ringer＇s EP solution （EP was diluted in Ringer＇s solution, and the concentration was 3.26 g/L） by intravenous injection via dorsal penile vein, then they underwent the non-lethal segmental hepatic warm ischemia. The blood samples from inferior vena cava were collected at 2, 8, 24 and 48 hours after the establishment of model respectively, and the animals were sacrificed to get liver tissues. The changes of serum levels of alanine aminotransferase （ALT）, aspartate transaminase （AST）, and the contents of HMGB1, tumor necrosis factor-α （TNF-α） as well as interleukin-10 （IL-10） in hepatic tissues were determined at various time points. Results At 2 48 hours after I/R, serum ALT as well as AST levels in group B and C were significantly higher than those in normal controls. The serum ALT levels at every time point and serum AST levels at 2 hours and 8 hour5 in group C were markedly lower than those in group B （P〈0.05 or P〈0.01）. At 89 24 and 48 hours, the liver levels of HMGB1 in group B were significantly higher than those in normal controls, while the liver HMGB1 level in group C was only at 48 hours significantly higher than that in normal controls. At 8 hours and 24 hours, the HMGB1 levels in group C were lower than those in group B markedly. TNF-?