高原低氧对大鼠肝脏氧化应激损伤的研究

The research of hepatic oxidative stress injury in high altitude hypoxia in rats

目的模拟高原低压、低氧环境建立大鼠缺氧模型,探讨不同缺氧时间对大鼠缺氧肝损伤程度的影响。方法采用国产低压低氧动物实验舱模拟海拔6 000 m高原缺氧环境,观察1 d、3 d、5 d、7 d不同缺氧时间大鼠组织病理学变化情况,并测定血浆丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)的变化及丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性的变化。结果 ALT、AST、ALP、MDA随缺氧时间的延长而升高,尤其以5 d、7 d缺氧组升高明显(P<0.05),SOD活性明显下降(P<0.05),并可见组织形态发生明显改变。结论高原低压低氧环境能引起大鼠肝脏发生氧化应激反应而导致肝损伤,其损伤程度随时间延长而加重,该模型为下一步研究高原脂肪肝的发病机制及防治提供基础。

Objective To establish an animal model of mountain sickness by a decompression chamber and to inves- tigate the effect of different hypoxia durations on the injury degree of liver in experimental rat. Methods Rats were housed in a decompression chamber and exposed to simulated high altitude of 6 000 meters for 1 day, 3 days, 5 days, 7 days, respectively. Pathological changes, the serum MDA content, ALT, AST, ALP activity and SOD activity were ex- amined. Results The serum MDA content, ALT, AST, ALP activity were gradually increased with time expanded of hypoxia, especially in 5 days, 7 days, the SOD activity was obviously decreased （P 〈 0.05）. Pathological changes of liver tissues were obvious. Conclusion High altitude hypoxia can induce liver oxidative stress and cause liver damage in rat. The injury was aggravated with time expanded of hypoxia. This model provides the basis for the mechanism study of fatty liver and its prevention and control.