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目的 :观察睡眠剥夺后大鼠脑组织SOD含量的影响 ,探讨睡眠剥夺引起的脑损害机制及干预药物的作用。方法 :采用小平台水环境法 (FlowerPot)制作大鼠睡眠剥夺模型 ,以黄嘌呤氧化酶法测定睡眠剥夺后大鼠额叶、海马、脑干和下丘脑SOD含量变化 ,并观察黄芪干预对SOD活性的影响。结果 :睡眠剥夺 3d后大鼠脑额叶、海马、中脑和下丘脑的SOD活性分别为 (44 .3±5 .9)、(47.5± 7.8)、(5 7.8± 6 .0 )、(6 4.5± 6 .8)、NU·mgpro 1高于正常对照组的 (16 .7± 5 .8)、(11.3± 2 .8)、(2 0 .3± 3.8)和 (17.0± 5 .7)NU·mgpro 1(P <0 .0 1)。经黄芪干预后额叶、海马、中脑及下丘脑SOD活性分别降为 (31.3± 5 .7)、(2 7.3± 5 .8)、(32 .8± 6 .9)、(31.7± 7.8)NU·mgpro 1,低于生理盐水对照的 (46 .9± 5 .8)、(5 1.3± 10 .4 )、(5 9.4± 7.6 )和 (5 9.6± 8.3)NU·mgpro 1(P <0 .0 1)。结论 :睡眠剥夺过程可能存在自由基损害影响 ,黄芪有一定的抗氧化应激作用
OBJECTIVE: To observe the effect of sleep deprivation on the content of SOD in brain tissue of rats and explore the mechanism of sleep deprivation-induced brain damage and the effect of intervention drugs. Methods: The rat sleep deprivation model was made by using Flowerpot. The content of SOD in frontal lobe, hippocampus, brainstem and hypothalamus of rats after sleep deprivation was measured by xanthine oxidase method. The effects of astragalus on SOD Effect of activity. RESULTS: The SOD activity in frontal lobe, hippocampus, midbrain and hypothalamus of rats after sleep deprivation for 3 days were (44.3 ± 5.9), (47.5 ± 7.8), (7.88 ± 6.0), ( 6 4.5 ± 6 .8), NU · mgpro 1 was higher than that of the control group (16.7 ± 5 .8), (11.3 ± 2 .8), (20.3 ± 3.8) and (17.0 ± 5. 7) NU · mgpro 1 (P <0 .01). The activity of SOD in the frontal lobe, hippocampus, midbrain and hypothalamus were reduced to (31.3 ± 5.7), (32.3 ± 5.5), (32.8 ± 6.9), (31.7 ± 7.8 ) NU · mgpro 1, (46.9 ± 5 .8), (5 1.3 ± 10 .4), (5 9.4 ± 7.6) and (5 9.6 ± 8.3) NU · mgpro 1 (P <0 .0 1). Conclusion: The sleep deprivation process may have the impact of free radical damage, astragalus has some anti-oxidative stress