Gallic Acid Ameliorates Cognitive Impairment Caused by Sleep Deprivation through Antioxidant Effect

作者：Xiaogang Pang, Yifan Xu, Shuoxin Xie, Tianshu Zhang, Lin Cong, Yuchen Qi, Lubing Liu, Qingjun Li, Mei Mo, Guimei Wang, Xiuwei Du, Hui Shen, Yuanyuan Li · 发表于：Experimental Neurobiology · 年份：2023 · DOI：10.5607/en23015 · 被引用次数：11 · 研究领域：Neuroinflammation and Neurodegeneration Mechanisms、Olfactory and Sensory Function Studies、Neuroscience and Neuropharmacology Research

transients while increasing the proportions of inactive neurons. Following the cessation of sleep deprivation, neuronal calcium transients demonstrated a gradual recovery. Moreover, whole-cell patch-clamp recordings revealed a significant decrease in the frequency of spontaneous excitatory post-synaptic current (sEPSC) after SD. The investigation also assessed several oxidative stress parameters, finding that sleep deprivation substantially elevated the level of malondialdehyde (MDA), while simultaneously decreasing the expression of Nuclear Factor erythroid 2-Related Factor 2 (Nrf2) and activities of Superoxide dismutase (SOD) in the ACC. Importantly, the administration of gallic acid (GA) notably mitigated the decline of calcium transients in ACC neurons. GA was also shown to alleviate oxidative stress in the brain and improve cognitive impairment caused by sleep deprivation. These findings indicate that the calcium transients of ACC neurons experience a continuous decline during sleep deprivation, a process that is reversible. GA may serve as a potential candidate agent for the prevention and treatment of cognitive impairment induced by sleep deprivation.