Objective To study the effects of ginsenosides (GS) on spontaneous sleep architecture and Cortical EEG power spectrum. Methods 24 adult SD rats were randomly divided into the control, GS 10 and 100mg/kg groups ( n = 8). Rats were instrumented with sleep-wake recording electrodes. After recovery from surgical operation,rats were orally administered GS 10 and 100mg/kg or distilled water once per day for 6 days. On GS administration day 1 and 6,Polygraphic signs of undisturbed sleep-wake activities were recorded for 12 h after GS administration. Results On GS administration day 1 ,only 100mg/kg GS increased significantly total sleep and the non-rapid eye movement ( NREM ) sleep but decreased wakefulness [(9.40 ± 0.88 ) h, ( 8.00 ± 1. 21 ) h,(2.46 ±0.81)h s (7.55 ±1.59)h,(6.36±1.54)h,(4.38 ±1.62)h,(P＜0.01, P＜0.05, P＜0.01),respectively] ;Low and high dose GS enhanced δ-wave power of NREM sleep and wakefulness (P＜ 0.05 ) but reduced θ-wave power of wakefulness (P＜0.01) and-wave power during NREM, REM sleep and wakefulness (P ＜ 0.01 ),moreover,Low and high dose GS lowered θ-wave power of REM and NREM stage(P＜0.05 ) ,respectively. After 6days of GS administration, Low and high dose GS increased markedly total sleep(P＜0.05 ) and NREM sleep(P＜0.05 ) but decreased wakefulness (P ＜0.05 ) and sleep-wake cycles (P ＜ 0.05, P ＜ 0.01 ); moreover, Low and high dose GS enhanced δ-wave power during NREM sleep and wakefulness (P ＜ 0. 05 ) but reduced θ-wave power of wakefulness(P ＜ 0.05 ) and -wave power during NREM, NEM sleep and wakefulness (P ＜ 0. 05 ), 10mg/kg GS also lowered θ-wave power of NREM sleep (P＜0.01). Conclusion These results demonstrate that GS can regulate spontaneous sleep architecture in time dependent manner,as well as cortical EEG power spectrum in rats.

Endothelial dysfunction was closely related with AS , NO bioavailability ( production and utilization of endothelial NO ) was decreased by oxidative stress , lipid infiltration , inflammatory factor expression , vascular tone alteration and so on , which play an important role in endothelial dysfunction .Enhanced arginine , activityand asym-metric dimethylarginine together with increased hyperhomocysteinemia all promote AS by intervening NO bioavail -ability.Diabetes mellitus, obesity, chronic kidney disease , smoking and so on also involved in AS via influencing NO bioavailability and NO level .

Adult rats were implanted with sleep-wake recording electrodes in our experiments. Polygraphic signs of undisturbed sleep-wake activities were recorded for 24 h before cocaine administration, cocaine withdrawal day 1 (acute), day 8 (subacute), and day 14 (subchronic). Western blot method was performed to examine the expression levels of adenosine receptor subtypes in hypothalamus and cerebellum. Non rapid eye movement (NREM) sleep was significantly increased during nighttime (P < 0.01) and daytime (P < 0.05) on withdrawal day 8. The increase of NREM sleep was significant during nighttime (P < 0.01) and slight during daytime on withdrawal day 14, whereas both daytime and nighttime rapid eye movement (REM) sleeps were reduced markedly (P < 0.01) on withdrawal day 8 and 14. In addition, A2A receptor level was significantly enhanced on cocaine withdrawal day 8 and day 14 (P < 0.05), whereas A1 receptor level reduced markedly on withdrawal day 14 (P < 0.05). However, compared with that in the control group, no significant changes existed among adenosine A1, A2A and A2B receptors in rat cerebellum on cocaine withdrawal day 1, day 8 and day 14. Our findings suggest that sleep disorder caused by subacute and subchronic cocaine abstinence may be associated with over-expression of adenosine A2A receptor in rat hypothalamus to some extent.
Animals ; Cocaine ; adverse effects ; Dyssomnias ; chemically induced ; Electroencephalography ; Hypothalamus ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Receptor, Adenosine A2A ; metabolism ; Substance Withdrawal Syndrome

Sleep disorders commonly exist and are the earliest clinical symptoms in Alzheimer's disease (AD). At present, the molecular mechanism of AD caused by sleep disorders is not clear. Recent studies have found that sleep disorders can promote the accumulation of beta amyloid (Aβ) in the brain to form amyloid plaques with toxic effects. The increased Aβ inhibits the synaptic transmission pathway and induces abnormal phosphorylation of tau protein, which eventually leads to synaptic dysfunction. In addition, the inflammatory and stress response induced by Aβ are also associated with AD. Therefore, the improvement of sleep disorders may be a new pathway for the treatment of AD, in which light therapy is proved to be particularly effective. This article reviewes the latest progresses in the influences of sleep disorders in pathogenesis and treatment of AD in recent years.

Alzheimer's disease (AD) is characterized byβ-amyloid (Aβ) deposition and tauprotein hyperphosphorylation, whereas its pathogenesis has not been fully known so far. The metabolism of Aβand tau protein is critically affected by autophagy. In the early phase of AD, Aβand tau protein can induce themselves to be eliminated via mTOR-dependent and independent autophagy pathways. In addition, transcription factors EB and apolipoprotein E4 also regulate autophagy and thus participate in the metabolism of Aβand tau protein, affecting AD progression. This review summarized the roles of autophagy in the metabolism of Aβand tau protein and the autophagy regulators closely related to AD in the recent studies.