摘要
目的:评估睡眠剥夺(SD)后大鼠心肌组织损伤程度并探讨其机制。方法:将60只实验大鼠随机分为6组,每组10只。采用改良的多平台SD法(MMPM)建立SD模型,观察SD对心肌组织中缺血修饰白蛋白(IMA)、高敏C反应蛋白(hs-CRP)、还原型谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物酶(SOD)含量的影响。结果:与笼养组(CC组)和大平台组(TC组)相比,SD后大鼠心肌组织中IMA、hs-CRP、GSH及MDA的含量明显升高(P<0.05),且随着SD时间的延长有明显上升的趋势;而SOD的活性随着SD时间的延长有降低的趋势。结论:SD可引起大鼠心肌发生明显的氧化应激和炎症反应,且随着氧化应激和炎症反应的加重,心肌发生进行性缺血缺氧损害。
AIM：To evaluate the severity of myocardial damage after sleep deprivation and to explore its mechanism. METHODS： Sixty rats were randomized into six groups （ten in each group） and sleep deprivation rat models were established by “multi-platform method” （MMPM）. Effects of sleep deprivation on the contents of ischemia modified albumin （IMA）, high-sensitivity C-reactive protein （hs-CRP）, glutathione （GSH）, superoxide dismutase （SOD） and malondialdehyde （MDA） in rat myocardium were evaluated. RESULTS： Compared with those in the normal cage control （CC） and tank control （TC） group, the contents of IMA, hs-CRP, GSH and MDA increased （P〈0.05）. With the elongation of sleep deprivation time, the contents of these markers increased, but the activity of SOD showed a decreasing tendency. CONCLUSION： Sleep deprivation contributes to rat myocardial oxidative stress and inflammation. With the aggravating oxidative stress and inflammation, the damaging effects of ischemia and hypoxia on myocardium become more serious.
出处
《心脏杂志》
CAS
2011年第5期598-600,共3页
Chinese Heart Journal
关键词
睡眠剥夺
心肌损伤
氧化应激
炎症
大鼠
sleep deprivation
myocardial damage
oxidative stress
inflammation
