深慢波睡眠剥夺对大鼠睾丸组织氧化应激反应的影响

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目的:研究深慢波睡眠剥夺对大鼠睾丸组织氧化应激反应的影响。方法:36只5周龄健康雄性Wistar大鼠,随机分为深慢波睡眠时相剥夺组(SD1组)、深慢波睡眠时相及时长剥夺组(SD2组)和空白对照组(CC组),每组12只,利用小平台水环境建立深慢波睡眠剥夺模型。SD1组每间隔24 min干扰1次,SD2组每间隔24min剥夺睡眠8 min;夜间都进行12 h的完全睡眠剥夺。CC组模拟正常的12 h光照、12 h黑暗时间。28 d后,大鼠股动脉放血,留取睾丸组织进行称重,测定睾丸组织中蛋白含量、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物岐化酶(SOD)水平,显微镜下观察睾丸病理结构的改变。结果:SD1、SD2组大鼠的终末体质量[(248.1±25.1)g、(232.9±10.1)g]均下降,与CC组[(268.5±1.6)g]相比差异有统计学意义(P均<0.05);与CC组相比,SD2组睾丸相对质量明显升高[(54.9±3.5)×10~(-2)vs(50.0±1.3)×10~(-2),P<0.05]。与CC组相比,SD2组睾丸组织蛋白含量、MDA含量、SOD活性和GSH-Px均有显著差异[蛋白含量:(4.5±0.9)g pro/L vs 6.3±1.4)g pro/L;MDA含量:(1.3±0.3)nmol/mg pro vs(1.1±0.1)nmol/mg pro;SOD活性:(135.2±26.9)U/mg pro vs(104.3±33.1)U/mg pro;GSH-Px活性:(21.7±4.3)U/mg pro vs(15.6±4.0)U/mg pro,P均<0.05],而与SD1组比较差异无统计学意义。SD1组睾丸病理学改变不明显,但SD2组睾丸生精小管管腔变小,周围间质部分增加,间质充血水肿明显。结论:长期深慢波睡眠剥夺对大鼠睾丸组织结构产生损伤并引起氧化应激反应。 Objective: To study the effects of deep sleep slow wave sleep deprivation on oxidative stress in testis of rats. Methods: Thirty-six healthy male Wistar rats aged 5 weeks were randomly divided into two groups: SD-SD group, SD-SD group, SD2-SD group and CC group ), 12 in each group. The deep-sleep-wave sleep deprivation model was established by the water environment of the small platform. SD1 group every 24 min interference 1 time, SD2 group every 24 min sleep deprivation 8 min; at night were 12 h sleep deprivation. CC group simulated normal 12 h light, 12 h dark time. After 28 days, the femoral arteries were exsanguinated and the testicular tissues were collected and weighed. The contents of protein, malondialdehyde (MDA), glutathione peroxidase (GSH-Px), superoxide dismutase Enzyme (SOD) levels were observed under microscope microscope pathological changes. Results: The final body weight of rats in SD1 and SD2 group was significantly lower than that in CC group ([(248.1 ± 25.1) g, (232.9 ± 10.1) g] [(268.5 ± 1.6) g] P <0.05). Compared with CC group, the relative mass of testis in SD2 group was significantly higher than that in CC group [(54.9 ± 3.5) × 10 ~ (-2) vs (50.0 ± 1.3) × 10 ~ (-2) ]. Compared with CC group, there was a significant difference in testis tissue protein content, MDA content, SOD activity and GSH-Px in SD2 group [protein content: (4.5 ± 0.9) g pro / L vs 6.3 ± 1.4) g pro / (1.3 ± 0.3) nmol / mg pro vs (1.1 ± 0.1) nmol / mg pro; SOD activity: (135.2 ± 26.9) U / mg pro vs (104.3 ± 33.1) U / mg pro; GSH-Px activity: (21.7 ± 4.3) U / mg pro vs (15.6 ± 4.0) U / mg pro, all P <0.05], but no significant difference compared with SD1 group. The pathological changes of testis in SD1 group were not obvious, but the seminiferous tubules of SD2 group became smaller, the surrounding mesenchyma increased and interstitial congestion and edema were obvious. Conclusion: Long-term deep and slow wave sleep deprivation can damage the structure of testis and cause oxidative stress.
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