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Syringin may exert sleep‐potentiating effects through the NOS / NO pathway
Author(s) -
Cui Yue,
Zhang Ying,
Liu Gang
Publication year - 2015
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/fcp.12095
Subject(s) - nitric oxide synthase , sleep (system call) , nitric oxide , sleep onset latency , endocrinology , pharmacology , medicine , latency (audio) , sleep onset , insomnia , computer science , operating system , engineering , electrical engineering
Sleep is essential for basic survival as well as for optimal physical and cognitive performance in both human beings and animals. To investigate the effect of syringin on sleep of anesthetized mice and the potential mechanisms, 35 male K unming mice were randomly divided into six experimental groups ( n = 5) and one control group ( n = 5). Sleep latency and sleep duration, as well as nitric oxide ( NO ) content and nitric oxide synthase ( NOS ) activity, were determined after syringin administration. The NO precursor l ‐ A rginine ( l ‐ A rg) or NOS inhibitor NG ‐ N itro‐ l ‐ a rginine methyl ester ( l ‐ NAME ) was administered alone or in combination with syringin, and time for sleep latency and duration was recorded. After intragastric administration of syringin, sleep latency decreased in a dose‐ and time‐dependent manner, concomitant with increased sleep duration. The optimal sleep performance was obtained when syringin was given at a dose of 80 mg/kg for eight consecutive days. Syringin significantly reduced NO concentration and NOS activity. Administration of l ‐ A rg prolonged sleep latency and shortened sleep duration, and the effects were fully reversed by syringin coadministration. Administration of L ‐ NAME induced a significant reduction in sleep latency and a corresponding increase in sleep duration, and coadministration of syringin further enhanced the effects. The finding of our study demonstrated that syringin could exert sleep‐potentiating effects on anesthetized mice in a time‐ and dose‐dependent manner, and these effects may be intimately correlated with the NO / NOS pathway.