慢性间隙性缺氧对大鼠心肌氧化应激影响

Effect of chronic intermittent hypoxia on oxidative stress in the myocardial muscles of rats

摘要:

目的：通过建立模拟阻塞性睡眠呼吸暂停低通气综合征（Obstructive sleep apnea hypopnea syndrome，OSAHS）的慢性间歇缺氧（Chronic intermittent hypoxia，CIH）的大鼠动物模型，观察CIH对大鼠心肌氧化应激（Oxidative stress，OS）的损伤及复氧后的改变。方法：建立16只慢性间隙性缺氧大鼠模型，其中8只缺氧后复氧，采用比色法、免疫印迹等方法测定其心肌还原型谷胱甘肽（Glutathione，GSH）、蛋白质羰基化（Protein carbonylation，PC），并与8只正常大鼠进行比较。结果：慢性间隙性缺氧模型大鼠心肌还原型谷胱甘肽明显低于对照组（P<0.05），蛋白质羰基化水平明显高于对照组（P<0.05）；复氧组大鼠心肌还原型谷胱甘肽，ＰＣ水平与对照组相比无明显差异（P>0.05）。结论：慢性间隙性缺氧模型的大鼠心肌ＯＳ水平升高，并伴有蛋白质ＯＳ损伤，复氧后OS水平降低。

Abstract:

Objective：To establish the chronic intermittent hypoxia （CIH） rat animal model Dv simulation of obstructive sleep ap－nea-hypopnea syndrome（OSAHS），and to observe the effect of CIH on oxidative stress in rat myocardial injury and reoxygenation.Methods：Chronic intermittent hypoxia rat model with 16 rats were established，in which eight rats were reoxygenated after hypoxia. Glutathione（GSH） and protein carbonylation of heart muscles were determined with the method of Western blot，and then were com－pared with those of eight normal rats. Results：The glutathione of myocardial muscles were significantly decreased in chronic inter－mittent hypoxia group compared with that in control group（P<0.05）. However，the protein carbonylation levels were significantly high－er （P<0.05）. Compared with those in the control group，the glutathione and protein carbonylation levels of the reoxygenation group had no significant difference（P>0.05）. Conclusion：Oxidative stress level increase and modification of proteins takes place in myocar－dial muscle of rats with chronic intermittent hypoxia. After reoxygenation，the oxidative stress level returns to normal.