摘要
目的从基因表达水平探讨心肌缺血／再灌注期间微量元素硒（Se）拮抗自由基损伤的机理。方法采用生化、原子吸收、RT-PCR、基因测序等技术，分别对对照组、口服有机硒、无机硒等3组心肌缺血／再灌注模型大鼠（每组20只）于缺血前、缺血30分钟、再灌注30分钟时的心肌丙二醛（MDA）含量、谷胱甘肽过氧化物酶（GSH-Px）活性、Se、Ca(2+)、Mg(2+)等离子浓度、GSH-PxmRNA水平及GSH-PxcDNA序列进行测定和组间比较。结果尽管服硒7天未引起两服硒组血浆和血细胞硒含量明显变化；但于缺血及再灌注后两组心肌GSH-Px活性和硒浓度明显增加、MDA改变程度低于对照组，再灌注后心肌GSH-PxmRNA水平增加而GSH-PxcDNA序列正常。结论补硒组通过提高再灌注30分钟内心肌的硒含量、GSH-Px表达水平及活性、减轻Ca(2+)超载程度，拮抗了自由基对心肌细胞的脂质过氧化损伤。
Objective To investigate the mechanism of selenium (Se) protecting against free radical damages during myocardial ischemia/reperfusion (I/R) in rats. Methods AII rats were separated into three groups: control, organic Se and inorganic Se supplemented groups. Myocardial I/R was established by operation in all three groups. Biochemical assays, atomic absorption spectrophotometry, RT-PCR and cDNA sequence scanning were performed to examine the changes in myocardial MDA level, GSH-Px artivity and gene expression, GSH-Px cDNA nucleotide sequence, as well as Se and Ca2+ and Mg2+ concentrations in the heart muscle during I/R.Results The administration of Se for 7 days did not significantly change the content of Se in the plasma and blood cells. In the two Se-supplemented groups, after reperfusion for 30 minutes, myocarial Se concentration and GSHPx activity were increased significantly, and GSH-Px expression was elevated with a normal cDNA sequence, and at the same time, MDA contents in the two Se-supplemented groups were lower than that in the control group.Conslusion Se supplementation can protect against free radical damages during myocardial I/R by increasing myocardial Se content and improving both the expression and activity of GSH-Px.
出处
《中华医学杂志》
CAS
CSCD
北大核心
1999年第11期852-856,共5页
National Medical Journal of China
基金
国家自然科学基金!39270199
北京市自然科学基金!7942013
关键词
硒
再灌注损伤
基因表达
心肌缺血
Selenium,Reperfusion injury,Myocardial,Gene expression
