Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences (CAAS), Beijing, China.
College of Food Science, Fujian Agriculture and Forestry University, Fuzhou, China.
Phytother Res. 2022 May;36(5):2072-2080. doi: 10.1002/ptr.7354. Epub 2022 Apr 3.
Mounting evidence suggests that there is a close association between chronic sleep deprivation (CSD) and cognitive deficits. The animal model of CSD-induced cognitive deficits is commonly used to seek potential treatments. Soy isoflavones (SI) have been reported to possess antioxidant, anti-inflammation, and neuroprotective effects. In the present study, the effects of SI on CSD-induced memory impairment were investigated. The mice were subjected to the sleep interruption apparatus and continuously sleep deprived for 2 weeks, while orally administrated with SI (10, 20, and 40 mg/kg) or Modafinil (MOD,100 mg/kg) during the CSD process. Immediately after the SD protocol, cognitive performance of mice was evaluated by the object location recognition (OLR) test, the novel object recognition (NOR) test, and the Morris water maze (MWM) task, as well as the hippocampus, was extracted for evaluation of oxidative stress parameters and inflammation levels through biochemical parameter assay and western blotting analysis. The results showed that SI administration remarkably improved the cognitive performance of CSD-treated mice in OLR, NOR, and MWM tests. In addition, SI significantly elevated total antioxidant capacity and superoxide dismutase enzyme activities, decreased malondialdehyde level, promoting antioxidant element nuclear erythroid-2-related factor 2, and its downstream targets, including heme oxygenase 1, and quinone oxidoreductase 1 protein expressions. Moreover, SI treatment significantly suppressed nuclear factor kappa B p65, nitric oxide synthase, and cyclooxygenase 2 activation, as well as the pro-inflammatory cytokines (Tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and interleukin-1β [IL-1β]) release in the hippocampus of CSD-treated mice. In summary, the current study provides an insight into the potential of SI in treatment of cognitive deficits by CSD.
越来越多的证据表明，慢性睡眠剥夺 (CSD) 与认知缺陷密切相关。CSD 诱导的认知缺陷动物模型通常用于寻找潜在的治疗方法。大豆异黄酮 (SI) 具有抗氧化、抗炎和神经保护作用。本研究探讨了 SI 对 CSD 诱导的记忆障碍的影响。小鼠连续接受睡眠中断装置睡眠剥夺 2 周，同时在 CSD 过程中口服给予 SI（10、20 和 40mg/kg）或莫达非尼 (MOD，100mg/kg)。SD 方案结束后，立即通过物体位置识别 (OLR) 测试、新物体识别 (NOR) 测试和 Morris 水迷宫 (MWM) 任务评估小鼠的认知表现，并提取海马进行评估通过生化参数测定和 Western blot 分析评估氧化应激参数和炎症水平。结果表明，SI 给药可显著改善 CSD 处理小鼠在 OLR、NOR 和 MWM 测试中的认知表现。此外，SI 显著提高总抗氧化能力和超氧化物歧化酶酶活性，降低丙二醛水平，促进抗氧化元素核红细胞 2 相关因子 2 及其下游靶标血红素加氧酶 1 和醌氧化还原酶 1 蛋白的表达。此外，SI 治疗可显著抑制 CSD 处理小鼠海马中核因子 kappa B p65、一氧化氮合酶和环氧化酶 2 的激活以及促炎细胞因子 (肿瘤坏死因子-α [TNF-α]、白细胞介素-6 [IL-6] 和白细胞介素-1β [IL-1β]) 的释放。综上所述，本研究为 SI 在治疗 CSD 引起的认知缺陷方面的潜力提供了新的见解。
