S-腺苷蛋氨酸对大鼠缺血再灌注肝线粒体超微结构的影响

S-adenosylmethionine affects mitochondrial ultrastructure of ischemic-reperfusion injury in rat liver

关键词:  腺苷蛋氨酸  缺血/再灌注  线粒体  超微结构

Key words:  S-adenosylmethionine  ischemia/reperfusion  mitochondrial  ultrastructure

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超微结构的影响。［方法］大鼠随机分为对照组（A组）、I/R组（B组）和SAM处理组（C组），SAM组大鼠在缺血再灌注前2 h先行腹腔注射SAM预处理。三组动物在阻断肝门30 min后（A组仅做分离，不阻断肝门），于再灌注0、1、6 h抽取下腔静脉血检测ALT、AST，切取肝组织用电镜观察线粒体的超微结构及制备线粒体匀浆检测SOD、MDA。［结果］再灌注1 h，B组MDA （5.15±0.33） nmol/mg、SOD（29.73±4.48 ）u/mg；C组MDA（4.57±0.15 ）nmol/mg、SOD（36.61±3.09 ）u/mg。再灌注6h，B组MDA（ 6.82±0.27） nmol/mg、SOD（23.86±1.68）u/mg；C组MDA（ 5.52±0.21 ）nmol/mg、SOD （28.38±2.18）u/mg。电镜下A组线粒体结构基本正常；B组线粒体数量减少，肿胀明显，部分细胞核固缩，可见凋亡小体；C组线粒体轻度肿胀，未见到细胞凋亡现象。［结论］SAM能抑制脂质过氧化反应，保护线粒体的形态和结构，肝细胞缺血再灌注后的损伤程度。

Abstract:

［Objective］To investigate the effect of SAM on the prevention of mitochondrial injury induced by hepatic ischemia and reperfusion. ［Methods］The rats were randomized into 3 groups:control group(A group)，I/R group (B group)，SAM-treated group（C group）.Rats were subjected to 30 min of hepatic ischemia and 0、1 and 6h of reperfusion(A group wasn’t subjected to hepatic ischemia). In the C group,2 h prior to ischemia, the animals received SAM intraperitoneally. The rats of every group were phlebotomized in the inferior cava vena to detect aspartate aminotransferase（AST） and alanine aminotransferase(ALT) of the serum, the liver specimens were observed ultrastructure and detected mitochondrial reduced super oxidedismutase (SOD) and Malondialdehyde(MDA).［Results］At 1h after reperfusion,in the B group MDA（5.15±0.33）nmol/mg，SOD （29.73±4.48）u/mg;in the C group MDA （4.57±0.15）nmol/mg，SOD（ 36.61±3.09）u/mg. At 6h after reperfusion,in the B group MDA （6.82±0.27）nmol/mg，SOD （23.86±1.68）u/mg;in the C group MDA （5.52±0.21）nmol/mg，SOD （28.38±2.18）u/mg.Observing with electron microscope,the mitochondria is natural in the A group,is severely decreasing and tumid in the B group，is slightly decreasing and tumid in the C group. The partial hepatic karyon formed small contractive body and there were small wizen bodys among hepatic cells in the B group.But these were restrained in the C group by SAM. ［Conclusions］SAM protects against mitochondrial injury, which prevents mitochondrial oxidant stress and improves ischemia-induced hepatic energy metabolism.