S-腺苷蛋氨酸对大鼠缺血再灌注肝脏能量代谢的影响  

Influence of S-Adenosylmethionine on Energy Metabolism of Mitochondrial Injury Induced by Ischemia-Reperfusion in Rat Liver

作　　者：郭志刚[1] 何晓顺[1] 熊俊[1] 朱晓峰[1] 王东平[1] 钱世鹍[1] 黄洁夫[1] 

机构地区：[1]中山大学附属第一医院器官移植中心,广州510080

出　　处：《中国普外基础与临床杂志》2007年第2期181-184,共4页Chinese Journal of Bases and Clinics In General Surgery

摘　　要：目的研究S-腺苷蛋氨酸(SAM)预处理对大鼠肝脏缺血再灌注损伤线粒体功能的影响。方法54只大鼠按随机数字表法随机均分为对照组、缺血再灌注组(I/R组)和SAM组,SAM组大鼠肝脏在缺血前2h行腹腔注射SAM预处理。3组动物在阻断肝门30min后(对照组仅做分离,不阻断肝门)复流,并于再灌注后0、1和6h抽取下腔静脉血检测ALT及AST,切取肝组织检测线粒体SOD、MDA、ATP及EC,并制备病理切片在电镜下观察线粒体的超微结构。结果再灌注后0、1及6h,I/R组ALT、AST和MDA明显高于对照组(P<0.01),SOD(除0h外)、ATP及EC明显低于对照组(P<0.01);SAM组ALT、AST及MDA(除0h外)明显低于I/R组(P<0.01),SOD(除0h外)、ATP及EC明显高于I/R组(P<0.05,P<0.01)。超微结构观察,I/R组线粒体较对照组有明显的损伤,线粒体数量减少,肿胀明显,嵴模糊不清,基质密度低;而SAM组与I/R组相比损伤程度明显减轻。结论SAM能抑制线粒体脂质过氧化反应,提高ATP的产生,最终提高线粒体的能量代谢水平,有效地减轻肝脏的缺血再灌注损伤。Objective To investigate the effect of S-adenosylmethionine （SAM） on mitochondrial injury that was induced by ischemia-reperfusion in rat liver. Methods Fifty-four rats were randomly divided equally into 3 groups： control group, ischemia-reperfuslon group （I/R group）, and SAM-treated group （SAM group）. Hepatic ischemia had been only lasted for 30 min by obstructing the blood stream of hepatic portal vena （the portal vena was only separated but not obstructed in control group）. The rats of SAM group received SAM intraperitoneally 2 h prior to ischemia. Blood samples of each group were collected from the inferior cava vena at 0, 1 and 6 h after reperfusion and the serum levels of AST and ALT were detected. Mitochondrial super oxidedismutase （SOD）, malondial dehyde （MDA）, adenosine triphosphate （ATP） and energy charge （EC） in samples of liver tissue were detected, and the mitochondrial ultrastructure was observed with electronmicroscope. Results The serum levels of AST, ALT and mitochondrial MDA at 0, 1 and 6 h after reperfusion in the I/R group were significantly higher than those in the control group, whereas the levels of mitochondrial SOD, ATP and EC were significantly lower than those in the control group （P〈0.01）. Except the value of 0 h, when it comes to SAM group, the levels of AST, ALT and mitochondrial MDA were significantly lower （P〈0.05） and the levels of mitochondrial SOD, ATP and EC were significantly higher （P〈0.05, P〈0.01） than those in the I/R group, respectively. The mitochondrial ultrastructure was injured obviously in I/R group when compared with that in control group. The number of mitochondria decreased and the mitochondria swelled, making the crista became obscure and the density of matrix became lower. The above changes in SAM group were less obvious when compared with those in I/R group. Conclusion SAM may protect mitochondrion against hepatic ischemia injury, since it may prevent mitochondrial lipid peroxidation, increase ATP, an

关 键 词：S-腺苷蛋氨酸 缺血再灌注 线粒体 能量代谢 

分 类 号：R657.3[医药卫生—外科学]