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目的:研究玛咖脂溶性提取物对睡眠剥夺造成的小鼠学习记忆力下降的影响,并对脂溶性成分进行分析。方法:将48只雄性昆明种小鼠随机分为空白组,睡眠剥夺组,玛咖脂溶性提取物低、高剂量(60,200 mg·kg~(-1))组,连续ig给药16 d。实验第13天采用小平台水环境法制备小鼠睡眠剥夺模型,以通道式水迷宫实验测试小鼠睡眠剥夺24,48,72 h的学习记忆能力,观察睡眠剥夺72 h后小鼠脑组织病理学变化并检测脑组织超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px),脂质过氧化物丙二醛(MDA)含量。用气相色谱-质谱仪(GC-MS)和高效液相色谱仪(HPLC)对玛咖脂溶性成分进行检测。结果:与空白组相比,睡眠剥夺组小鼠水迷宫潜伏期显著延长,盲端错误次数显著增加(P<0.05),补充玛咖脂溶性提取物高剂量可显著缩短小鼠在通道式水迷宫中的潜伏期(P<0.05),减少盲端错误次数;降低脑组织MDA含量(P<0.01),使SOD和GSH-Px活力恢复到正常水平;降低海马组织的损伤。结论:补充含有玛咖酰胺的脂溶性提取物可以缓解睡眠剥夺导致的小鼠学习记忆力的降低和海马组织的损伤,其机制可能与抑制脂质过氧化有关。
Objective: To study the effect of maca lipase-soluble extract on the decline of learning and memory in mice induced by sleep deprivation, and to analyze the fat-soluble components. Methods: Forty eight male Kunming mice were randomly divided into blank control group, sleep deprivation group and low-dose and high-dose (60,200 mg · kg -1) Macaol extract for 16 days. On the thirteenth day of experiment, mice sleep deprivation model was prepared by the small platform water environment method. The learning and memory ability of mice was detected by channel water maze test at 24,48,72 h after sleep deprivation. Neuroimmunology was used to detect the contents of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in brain tissue. The Caffeine-soluble fraction was detected by gas chromatography-mass spectrometry (GC-MS) and high performance liquid chromatography (HPLC). Results: Compared with the blank group, the latent period of water maze in the sleep deprivation group was significantly prolonged, the number of false positives in the blind end was significantly increased (P <0.05), and the high dose of macadamia extract could significantly reduce the latency of mice in the channel water maze (P <0.05), reduce the number of errors at the blind end, reduce the content of MDA in brain tissue (P <0.01), and restore the activity of SOD and GSH-Px to normal level, and reduce the damage of hippocampal tissue. CONCLUSION: Supplementation of the fat-soluble extract containing macaramide can alleviate the learning and memory impairment and damage of hippocampal tissue induced by sleep deprivation in rats. The mechanism may be related to the inhibition of lipid peroxidation.