缺血后处理对鼠肝缺血再灌注损伤细胞凋亡及Bcl-2和Bax表达的影响

目的观察缺血后处理对肝脏缺血再灌注损伤后早期肝组织细胞凋亡及Bcl-2和Bax表达的影响，并探讨其肝保护的机制。方法建立大鼠肝脏缺血再灌注模型，54只雄性SD大鼠随机分为假手术组（SO组）、缺血再灌注组（IR组）和缺血后处理组（IPC组）。以缺血再灌注前反复多次的短暂预再灌注及停灌注作为后处理。分别于再灌注后1、3、6h测定血清肝酶，SP免疫组化法测定肝脏Bcl-2和Bax表达水平，TUNEL法检测肝组织中凋亡细胞。结果与SO组相比，IR组肝酶活性升高，Bcl-2表达降低，Bax表达升高并可见明显的细胞凋亡；而IPC组同IR组相比，肝酶活性降低，Bcl-2表达升高，Bax表达降低，凋亡指数（AI）下降，差异均有统计学意义。结论缺血后处理对大鼠肝脏缺血再灌注损伤有明显的保护作用，可通过促进Bcl-2表达及抑制Bax表达而拮抗肝细胞凋亡，从而减轻肝脏缺血再灌注损伤。

Effect of ischemic postconditioning on cells apoptosis and Bcl-2 and Bax expression in rat liver after ischemia-reperfusion injury

Objective To investigate the effect of ischemic postconditioning（IPC） on apoptosis and the expression of Bcl-2 and Bax in hepatic tissue after early ischemia-reperfusion injury and its mechanism. Methods A rat model of acute hepatic ischemia- reperfusion was established. Fifty-four male Sprague-Dawley rats were randomly allocated into sham-operated （SO） group, ischemia-reperfusion（IR） group and ischemic postconditioning（IPC） group. IPC was achieved by several brief episodes of reperfusion before the persistent reperfusion procedure. The activity of plasma enzyme and expressions of Bcl-2 and Bax in hepatic tissue were measured respectively at 1, 3, 6 h after reperfusion. The apoptosis in hepatic tissue was assessed by TUNEL method. Results Compared with SO group, the activity of plasma enzyme and expression of Bax increased and the expression of Bcl-2 reduced in IR group. There were obvious apoptosis in IR group. While compared with IR group, the activity of plasma enzyme and expression of Bax were reduced and the expression of Bcl-2 was increased in IPC group. The apoptotic index in IPC group was lower than in IR group.The difference were statistically significant. Conclusions IPC can relieve the hepatic ischemia- reperfusion injury in rat liver. IPC may inhibit apoptosis in hepatic tissue by up-regulating Bcl-2 and down-regulating Bax, thus produce a protective effect on hepatic ischemia-reperfusion injury.