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目的通过建立大鼠模型并测定间歇低氧及持续低氧大鼠肝脏中过氧化产物丙二醛(MDA)水平,探讨睡眠呼吸暂停模式间歇低氧对大鼠肝脏氧化应激损伤的机制。方法雄性Wistar大鼠96只,随机分为3组:间歇低氧组(IH),持续低氧组(CH)和常氧对照组(SC)。分别于暴露第2、4、6、8周随机抽取8只大鼠麻醉处死,留取肝脏组织,应用化学比色方法检测大鼠肝脏MDA水平。结果大鼠肝脏MDA含量IH组明显高于CH组和SC组(均P<0.01),IH及CH组MDA水平随暴露时间延长逐渐增加。结论睡眠呼吸暂停模式间歇低氧能引起大鼠肝脏发生氧化应激反应而导致肝损伤,其损伤程度比持续低氧更为严重,且随时间延长而增加。
OBJECTIVE: To establish a rat model and determine the level of malondialdehyde (MDA) in the liver of rats with intermittent hypoxia and continuous hypoxia to explore the mechanism of oxidative stress induced by sleep apnea hypoxia in rat liver. Methods Ninety-six male Wistar rats were randomly divided into three groups: intermittent hypoxia group (IH), continuous hypoxia group (CH) and normoxic control group (SC). At the 2nd, 4th, 6th and 8th week, 8 rats were randomly selected and anesthetized. The liver tissue was collected and the liver MDA level was detected by chemical colorimetric method. Results The liver MDA content in IH group was significantly higher than that in CH group and SC group (all P <0.01). The levels of MDA in IH group and CH group increased gradually with the prolongation of exposure time. Conclusion Intermittent hypoxia caused by sleep apnea can cause oxidative stress in the liver of rats, leading to liver injury. The degree of damage is more serious than that of continuous hypoxia and increases with time.