目的

探讨缺血后处理（IPC）对大鼠肝脏缺血再灌注损伤早期的保护作用机理。

方法

建立大鼠肝脏缺血再灌注模型，54只健康雄性SD大鼠随机分为假手术组（SO组）、对照组（IR组）和缺血后处理组(IPC组)。后处理组于完全再灌注前，给予多次短暂复灌复停作为缺血后处理。分别于再灌注后1 h、3 h及6 h抽血进行血清ALT、AST活性及TNF-α表达测定，免疫组化测定肝脏NF-κB活性及ICAM-1的表达。

结果

与SO组比较，IR组及IPC组再灌注后大鼠血清ALT、AST活性明显增高，肝脏NF-κB活性明显增强，TNF-α和ICAM-1表达也随之增加；同IR组相比，IPC组的血清ALT、AST活性明显降低，NF-κB活性及TNF-α和ICAM-1表达亦明显降低，差异均具有统计学意义(P<0.01)。

结论

缺血后处理能够减轻肝脏缺血再灌注损伤。其保护作用可能与通过抑制再灌注早期NF-κB的活性，降低了TNF-α和ICAM-1等炎性细胞因子水平有关。

Objective

To study the protective role of ischemic postconditioning(IPC)against early ischemic-reperfusion injury in rat liver.

Methods

A rat model of acute hepatic ischemia-reperfusion was established. 54 healthy male Sprague-Dawley rats were randomly divided into sham-operated(SO)group,ischemia-reperfusion(IR)group and IPC group.IPC were achieved by several brief reperfusion-ischemia followed by persistent reperfusion. The activity of NF-κB and expressions of ICAM-1 in hepatic tissue were measured respectively at 1,3,6 h after reperfusion.Serum ALT,AST and TNF-αwere also determined respectively.

Results

Compared with SO group,the activity of hepatic NF-κB and serum ALT,AST increased in IR group and IPC group, while compared with IR group that was significantly attenuated in IPC group (P<0.01). Similarly, Serum levels of TNF-and hepatic levels of ICAM-1 were significantly elevated in IR group and were reduced in IPC group.

Conclusion

Ischemic postconditioning can relieve the ischemic reperfusion injury of rat liver.Thiss protective effect may be achieved through depressing NF-κB activation,cutting down cytokines contents.