Lu Cong, Wang Yan, Lv Jingwei, Jiang Ning, Fan Bei, Qu Lina, Li Yinghui, Chen Shanguang, Wang Fengzhong, Liu Xinmin
Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences (CAAS), Beijing 100193, China; Research Center for Pharmacology & Toxicology, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China.
Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences (CAAS), Beijing 100193, China.
Behav Brain Res. 2018 Sep 3;349:109-115. doi: 10.1016/j.bbr.2018.03.005. Epub 2018 Mar 12.
Sleep deprivation (SD) negatively caused cognitive deficit, which was associated with oxidative stress induced damage. Ginsenoside Rh2 had the ability to protect against damage caused by reactive oxygen species in vitro, showing antioxidant property. Therefore, it was hypothesized that Ginsenoside Rh2 could prevent SD-induced cognitive deficit via its antioxidant properties. In this study, the effect of Ginsenoside Rh2 on memory impairment induced by sleep deprivation was investigated. The mice were sleep deprived continuously for 14 days using our self-made Sleep Interruption Apparatus (SIA). Ginsenoside Rh2 was administered intraperitoneally at two doses (20 and 40 μmol/kg) for 20 days. Thereafter, behavioral studies were conducted to test the learning and memory ability using object location recognition (OLR) experiment and passive avoidance (PA) test. Additionally, the oxidative stress parameters in the serum and the brain tissues (cortex and hippocampus) were assessed, including the superoxide dismutase (SOD) enzyme activity, the total antioxidant reactivity (TAR), the malondialdehyde (MDA) level, the glutathione (GSH) level, and the lipid peroxidation (LPO) content. The results revealed that SD impaired both spatial and non-spatial memory (P < 0.05). Treatment with Ginsenoside Rh2 at both doses prevented memory impairment induced by SD. Moreover, Ginsenoside Rh2 normalized the reduction of SOD and TAR activities in the serum (P < 0.01) and the decrease of GSH content in both the cortex and hippocampus (P < 0.05) induced by SD. Furthermore, Ginsenoside Rh2 significantly decreased the MDA level in the serum (P < 0.05) and the LPO content in both the cortex and hippocampus (P < 0.05) compared to SD group. In conclusion, sleep deprivation impaired both spatial and non-spatial memory and Ginsenoside Rh2 reversed this impairment, probably by preventing the oxidative stress damage in the body, including the serum and brain during sleep deprivation.
睡眠剥夺（SD）会对认知功能产生负面影响，这与氧化应激诱导的损伤有关。人参皂苷Rh2在体外具有抵御活性氧所致损伤的能力，表现出抗氧化特性。因此，有人推测人参皂苷Rh2可通过其抗氧化特性预防睡眠剥夺诱导的认知缺陷。在本研究中，对人参皂苷Rh2对睡眠剥夺诱导的记忆损伤的作用进行了研究。使用自制的睡眠中断装置（SIA）对小鼠连续进行14天的睡眠剥夺。人参皂苷Rh2以两种剂量（20和40μmol/kg）腹腔注射给药20天。此后，进行行为学研究，使用物体位置识别（OLR）实验和被动回避（PA）测试来检测学习和记忆能力。此外，评估血清和脑组织（皮层和海马体）中的氧化应激参数，包括超氧化物歧化酶（SOD）活性、总抗氧化反应性（TAR）、丙二醛（MDA）水平、谷胱甘肽（GSH）水平和脂质过氧化（LPO）含量。结果显示，睡眠剥夺损害了空间记忆和非空间记忆（P<0.05）。两种剂量的人参皂苷Rh2治疗均预防了睡眠剥夺诱导的记忆损伤。此外，人参皂苷Rh2使睡眠剥夺诱导的血清中SOD和TAR活性降低（P<0.01）以及皮层和海马体中GSH含量降低（P<0.05）恢复正常。此外，与人参皂苷Rh2组相比，人参皂苷Rh2显著降低了血清中的MDA水平（P<0.05）以及皮层和海马体中的LPO含量（P<0.05）。总之，睡眠剥夺损害了空间记忆和非空间记忆，人参皂苷Rh2逆转了这种损伤，可能是通过预防睡眠剥夺期间包括血清和大脑在内的体内氧化应激损伤来实现的。
