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Disruption of the active phase of sleep alters the physiological homeostasis of the body and results in oxidative breakdown which may trigger a wide array of defects. The central nervous system and the metabolic system are some of the most affected systems as described in several literatures. Some plant based compounds with antioxidant property have been previously described in the abrogation of the deleterious effects of active sleep disruption. One of such compounds is quercetin. This study was premeditated to expatiate on the probable neuroprotective effect of quercetin on mice exposed to 72hr active sleep disruption. Mice were allotted into five treatment groups (n = 6): group 1 served as control, group 2 received 10 mL/kg vehicle, groups 3 and 4 received 25 and 50 mg/kg quercetin respectively, and group 5 received 50 mg/kg astaxanthin. Treatment lasted for 7 days while groups 2-5 were exposed to the sleep deprivation protocol starting from day 4. Behavioural tests followed by biochemical assays and histopathological changes in the prefrontal cortex were evaluated. Data were analysed by ANOVA set at p<0.05 significance. The results revealed that quercetin, in both doses, significantly amplified memory performance, attenuated depression-like behaviour, replenished catalase and superoxide dismutase, attenuated nitric oxide levels in brain and liver of mice when compared to control group and protected against loss of prefrontal cortex neurons. In conclusion, quercetin possesses protective effects against sleep deprivation-induced brain damage.

BackgroundStress, a known cause of neuropsychiatric disorders, is associated with cognitve dysfunction, neuroendocrine systems breakdown and altered brain oxidative status and proteins (Roozendaal, 2002; Radecki et al., 2005; Lupien et al., 2007). Apigenin (API), a natural flavonoid, with diverse biological activity, is thought to possess neuroprotective potentials (Li et al., 2015). This study investigated whether API administration abrogates chronic unpredictable mild stress (CUMS)‐induced cognitive impairment, as well as exploring its probable underlying mechanisms.MethodSwiss male mice (n = 10) were treated with API (12.5 ‐ 25 mg/kg, intraperitoneally) 30 min before exposure to CUMS daily for 14 days, thereafter tested for memory function using the Y‐maze and novel object recognition (NOR) tests. Levels of malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), and corticosterone levels were assessed using enzyme‐linked immunosorbent assay. The expressions of brain derived neurotrophic factor (BDNF), phosphorylated extracellular signal‐regulated kinase (pERK), and cAMP response element‐binding protein (pCREB) were assessed using immunohistochemistry.ResultCUMS produced cognitive impairment in mice as shown in the Y‐maze and NOR tests. CUMS significantly elevated MDA, and serum corticosterone levels, including reducing GSH and SOD levels, decreasing BDNF, pERK, and pCREB levels in the prefrontal cortex and hippocampus. However, chronic administration of API significantly prevented all these CUMS‐induced behavioral and biochemical alterations.ConclusionAPI may be a potential therapeutic agent for cognitive disturbances as seen within the stress model and its neuroprotective effect was partly mediated by restoring oxidative status, serum corticosterone levels, up‐regulating BDNF, pCREB and pERK levels. References Lupien SJ, Maheu F, Tu M, Fiocco A, Schramek TE. The effects of stress and stress hormones on human cognition: implications for the field of brain and cognition. Brain Cogn 2007; 65:209‐37Roozendaal B. Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiol Learn Mem 2002;78: 578‐95Radecki DT, Brown LM, Martinez J, Teyler TJ. BDNF protects against stress‐induced impairments in spatial learning and memory and LTP. Hippocampus 2005;15: 246‐53.Li R, Zhao D, Qu R, Fu Q, Ma S. The effects of apigenin on lipopolysaccharide‐induced depressive‐like behavior in mice. Neuroscience letters. 2015 May 6;594:17‐22.