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目的 观察大鼠睡眠剥夺 (SD)后的脑损害情况。 方法 采用小平台水环境法建立SD模型 ,以大平台组 (TC)和正常笼养组 (CC)作为对照组 ,采用酶联免疫吸附法测定髓鞘碱性蛋白(MBP)含量、采用双抗体放射免疫法测定皮质醇含量。电镜观察海马神经细胞超微结构变化。 结果 与 CC和 TC组比较 ,SD 1d、3d和 5 d后血清皮质醇水平均增高 ,差异有显著性意义 ;SD 5 d后血清 MBP含量增高 ,差异有显著性意义 ,SD 1d、3d水平无显著性差异。TC组与正常对照组比较 ,血清皮质醇增高而 MBP水平无显著性差异。电镜下观察 SD 5 d组 CA3区锥体细胞形态不规则 ,结构疏松 ,髓鞘板层分离、线粒体肿胀、空泡变性。 结论 长时间 SD可能引起脑器质性损害。
Objective To observe the brain damage after sleep deprivation (SD) in rats. Methods SD model was established by using small platform water environment method. The macropod group (TC) and normal cage group (CC) were used as control group. MBP content was determined by enzyme linked immunosorbent assay (ELISA) Immunoassay for determination of cortisol content. Ultrastructural changes of hippocampal neurons under electron microscope. Results Compared with CC and TC groups, serum cortisol levels increased on day 1, day 3 and day 5 after SD, and the difference was significant. After 5 days of SD, serum MBP level increased significantly, with significant difference at SD 1d and 3d Significant difference. TC group compared with the normal control group, serum cortisol increased but MBP levels no significant difference. Under electron microscope, the morphology of pyramidal cells in CA3 area of SD 5 d group was irregular, with loose structure, separation of myelin sheath, mitochondria swelling and vacuolar degeneration. Conclusion Long-term SD may cause brain organic damage.