节点文献

铜过量小鼠肝损伤模型的建立及各项指标的观察研究

Establishment of Mice Model Of Liver Damaged Induced By Excessive Copper

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 李万立罗海吉邓红查龙应孙素霞

【机构】 南方医科大学公共卫生与热带医学学院营养与食品卫生学系

【摘要】 目的探讨昆明小鼠在不同剂量的铜负荷时所引起肝损伤的生化及铜含量和相关病理的改变。方法 32只昆明小鼠随机分为对照组和实验组,实验组以不同浓度的硫酸铜每日灌胃,16周后,观察肝组织中丙二醛(MDA)的含量、超氧化物歧化酶(SOD)以及谷胱甘肽过氧化物酶(GSH-PX)的活性,测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)以及血清和肝组织的铜含量,并做肝脏病理以及电镜检查。结果与正常对照组相比,实验组肝组织中MDA的含量明显升高(p<0.001),而SOD和GSH-PX的活性明显下降(p<0.05);ALT、AST和血清铜含量明显升高(p<0.05);病理组织学检查可见实验组肝细胞变性坏死以及少量铜颗粒沉积;电镜提示肝细胞核、线粒体等细胞器异常,并可见铜颗粒。结论过量的铜可对肝脏造成损害,其机制可能与释放出的铜离子介导脂质过氧化而造成肝脏损害有关。其病变过程与Wilson病相似,可为进一步研究铜代谢异常等疾病提供动物模型,

【Abstract】 Objective To study the level of liver antioxygen and the liver pathological changs through intragastriced with different dose of CuS04 in mice.Method:32 mice were randomly divided into control group and experimental groups.The experimental groupes were intragastriced with different doses of CuS04 every day for 16 weeks.The levels of MDA,SOD and GSH-PX in the liver,ALT and AST in the blood-serums and copper were measured.Pathohistology analysis of the liver was also performed.Result:The level of MDA,ALT,AST and copper in liver were dramatically increased comparing with the control(p<0.05),and the levels of SOD and GSH-PX were significantly decreased(p<0.05).The pathohistology examination result showed that copper scattered in the experimental group and the necrosis of hepatic cells.Under electron microscope,the mitochondria was swelling and lysosome abnormal.Conclusion Excessive copper can cause severe damage of the liver.The mechanism may be the copperio which cause lipid peroxidation. This pathological changes are similar with Wilson disease,so as to provide further approach for the research of metabolization about copper.

【关键词】 肝损伤动物模型脂质过氧化
【Key words】 CopperLiver damageAnimal modelLipid peroxidation
  • 【会议录名称】 膳食营养、身体活动与健康——达能营养中心第十一次学术年会会议论文集
  • 【会议名称】膳食营养、身体活动与健康——达能营养中心第十一次学术年会
  • 【会议时间】2008-11-27
  • 【会议地点】中国广东广州
  • 【分类号】R742.4
  • 【主办单位】中国疾病预防控制中心达能营养中心
节点文献中: 

本文链接的文献网络图示:

本文的引文网络