摘要
目的探讨脓毒症对实验动物肝脏线粒体功能及结构的损伤机制。方法36只新西兰兔随机分成对照组、脓毒症组和脓毒症休克组,分别予生理盐水、脂多糖(LPS)1mg/kg、LPS2mg/kg静脉注射,制备脓毒症和脓毒症休克实验动物模型后提取肝脏线粒体,检测丙二醛(MDA)含量、ATP酶活性、线粒体肿胀程度和线粒体膜电位变化,同时观察肝脏线粒体超微结构变化。结果脓毒症组较对照组肝脏组织水肿加重,电镜见线粒体肿胀和膜增厚、MDA含量增高、ATP酶活性降低、线粒体膜流动性减低、膜电位差减小,且脓毒症休克组这些变化更加明显。结论脓毒症实验动物肝细胞线粒体膜脂质过氧化、抑制线粒体膜ATP酶活性、降低跨膜电位,使线粒体结构和功能受损,导致肝功能障碍。
Objective To study the effect of lipopolysaccharide on the function and the ultrastructure of hepatocellular mitochondrial membrane in septic rabbit. Methods 36 New Zealand white rabbits were randomly divided into three groups, control group（C） （n = 12）, sepsis group（S） （n = 12） and sepsis shock group （SS） （ n = 12）. The rabbits of control group , sepsis group and sepsis shock group were injected 0. 9% NaCl, lipopolysaccharide （LPS） 1 mg/kg and 2 mg/kg from vein separately. After animal model was prepared , liver mitochondria were isolated as soon as possible. The concentration of malondialdehyde （ MDA ） , the activity of ATPase, and the change of mitochondrial membrane potential were been tested, and ultrastructure of mitochondrial membrane was observed by electron microscope. Results The degree of liver edema and concentration of MDA , the activity of ATPase in S group was higher than that in C group, but change of potential and fluidity of mitochondrial membrane was lower in S group than that in C group. These changes became more significant in SS group. Conclusion LPS maybe damage hepatocellular mitochondrial function and structure, through peroxidizing lipid of mitochondrial membrane, inhibiting the activities of mitochondrial ATPase, reducing mitochondrial membrane potential and changing membrane fluidity, then induced acute liver dysfuntion.
出处
《中国急救医学》
CAS
CSCD
北大核心
2008年第2期147-150,共4页
Chinese Journal of Critical Care Medicine
基金
安徽高校省级自然科学研究项目(NoKJ2007B214)
关键词
脓毒症
肝细胞
线粒体
脂多糖
Sepsis
Liver cell
Mitochondrion
Lipopolysaccharide
