CAJ | 학술논문

目的观察大鼠肝移植术后早期肝组织内氧化还原因子1(redox factor-1,Ref-1)蛋白表达与肝脏损伤的关系.方法将150只Wistar大鼠动物分为三个组,肝移植组、假手术组和空白对照组.分别于肝移植术后3、6、9、12、24 h取材,采用免疫组织化学方法检测移植后各时间肝组织Ref-1蛋白表达,同时通过血清生化指标、组织病理学分析研究Ref-1蛋白表达的意义.结果血清学检查显示,肝移植术后3 h AST、ALT显著升高,术后6 h降低.病理学分析显示:术后24 h内,部分肝组织结构不清,肝细胞变性,肝窦扩张充血,炎细胞明显浸润.肝损伤较重.免疫组化检测显示,肝移植后早期肝实质细胞内Refl蛋白增高.9h达高峰,以后逐渐下降.结论肝移植术后发生肝损伤以术后6 h为最重,之后损伤程度逐渐减轻,这是由于移植术后缺血再灌注损伤,激活Ref-1的表达明显增加,修复了由于缺血再灌注损伤导致的细胞凋亡.
목적 관찰대서간이식술후조기간조직내양화환원인자1(redox factor-1,Ref-1)단백표체여간장손상적관계.방법 장150지Wistar대서동물분위삼개조,간이식조、가수술조화공백대조조.분별우간이식술후3、6、9、12、24 h취재,채용면역조직화학방법검측이식후각시간간조직Ref-1단백표체,동시통과혈청생화지표、조직병이학분석연구Ref-1단백표체적의의.결과 혈청학검사현시,간이식술후3 h AST、ALT현저승고,술후6 h강저.병이학분석현시:술후24 h내,부분간조직결구불청,간세포변성,간두확장충혈,염세포명현침윤.간손상교중.면역조화검측현시,간이식후조기간실질세포내Refl단백증고.9h체고봉,이후축점하강.결론 간이식술후발생간손상이술후6 h위최중,지후손상정도축점감경,저시유우이식술후결혈재관주손상,격활Ref-1적표체명현증가,수복료유우결혈재관주손상도치적세포조망.
Objective To study the relationship between graft injury and expression of redox factor-1 in early period after liver transplantation in rats. Methods One hundred and fifty adult male Wistar rats were randomly divided into three groups: liver transplant group, sham surgery group and control group. Animals were sacrificed in each group at different time points: 3,6,9, 12,24 hour after liver transplantation. The changes and significance of the expression of Ref-1 were explored by immunohistochemistry, serology and histopathology. Results Compared with sham surgery group and control group, the expression of Ref-1 protein in transplant group was higher than that in other two groups in early period after liver transplantation ( P ＜ 0. 05 ). In pathology there were lots of inflammation cells infiltration around the portal veins, and cell damage of hepatic tissue, while that in sham surgery and control group was comparatively slight. Serum ALT and AST values reached the peak at 6 ～ 12 h, and decreaced significantly after 12 h ( P ＜ 0. 05 ). Conclusions Graft injury after liver transplantation during early period reaches peak at 6 hour and then decreased. Hepatic ischemic reperfusion injury promotes Ref-1 expression, which in turn compensates for programme cell death induced by the injury.