目的：探讨缺血预处理（IP）减轻大鼠肝缺血再灌注（I/R）损伤的作用及机制。 方法：将15 只雄性SD 大鼠随机均分为假手术组、I/R 组、IP+I/R 组，采用Pringle 法制作肝I/R 模型 （缺血30 min+ 再灌注3 h），IP 采用I/R 前肝缺血10 min+ 再灌注10 min 诱导。各组大鼠于再灌注3 h 后处死取材，行肝组织病理学、血请谷草转氨酶（AST）、谷丙转氨酶（ALT）检测，同时检测肝组织 NF-κB 蛋白的表达，以及炎性细胞因子IL-1β、TNF-α 与氧化应激指标丙二醛（MDA）、髓过氧化 物酶（MPO）水平。 结果：除假手术组外，I/R 组与IP+I/R 组大鼠肝组织均出现肝损伤是病理学改变，IP+I/R 组的损伤程 度明显轻于I/R 组；与假手术组比较，I/R 组与IP+I/R 组大鼠血清AST、ALT 水平明显升高，肝组织 NF-κB 蛋白表达、IL-1β 与TNF-α 水平、MDA 与MPO 浓度均明显升高（均P<0.05），但IP+I/R 组 的各指标的升高幅度均明显小于I/R 组（均P<0.05）。 结论：IP 减轻大鼠肝I/R 损伤的作用与抑制NF-κB 活性，从而减轻炎症与氧化应激反应有关。
Influence of ischemic preconditioning on NF- B expression, and inflammatory and oxidative stress responses in rat liver tissue following ischemia-reperfusion
Objective: To investigate the alleviation effect of ischemic preconditioning (IP) on hepatic ischemia-reperfusion (I/R) injury in rats and the mechanism. Methods: Fifteen male SD rats were equally randomized into sham operation group, I/R group and IP plus I/ R group, respectively. I/R injury model was created by Pringle maneuver (30-min hepatic ischemia followed by 3-h reperfusion), and IP was induced by 10-min hepatic ischemia followed by 10-min reperfusion prior to I/R. Rats in each group were sacrificed and samples were collected after 3-h reperfusion, liver specimen pathological examination and measurement of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were performed, and meanwhile, the NF-κB protein expression, and the levels of inflammatory cytokines (IL-1β and TNF-α) as well as oxidative stress indexes that included malondialdehyde (MDA) and myeloperoxidase (MPO) in the liver tissues were determined. Results: Except in sham operation group, the liver tissues from either I/R group or IP plus I/R group showed pathological changes of liver injury, but the injury was milder in IP plus I/R group than that in I/R group. In both I/R group and IP plus I/R group compared with sham operation group, the serum AST and ALT levels, and liver tissue levels of NF-κB protein expression, IL-1β, TNF-α, MDA and MPO were all significantly increased (all P<0.05), but the increasing amplitudes of all these parameters in IP plus I/R group were significantly less than those in I/R group (all P<0.05). Conclusion: IP lessens hepatic I/R through inhibiting NF-κB activity, and thereby reduces inflammatory and oxidative stress responses.