RESUMO
Effect-directed isolation of free radical scavengers from the methanol extract of the freeze-dried fruiting bodies of the cultivated basidiomycetous mushroom, black poplar (Cyclocybe cylindracea), yielded a ß-carboline alkaloid. Its structure was determined based on ESI-TOF-MS/MS, NMR and circular dichroism spectra by comparison with published data. The compound, identified as the C1-S diastereomer of brunnein B, exhibited explicit radical scavenging activity (EC50â¯=â¯119.1⯱â¯1.2⯵g/mL). The quantity of the active component was determined with HPLC-MS in the fruiting body (36.2⯱â¯2.8â¯ng/g DW, dry weight) and its different tissues such as peel (94.7⯱â¯1.9â¯ng/g DW), inner cap (90.5⯱â¯1.3â¯ng/g DW), gills (71.5⯱â¯0.6â¯ng/g DW), and stipe (162.2⯱â¯1.7â¯ng/g DW). It is a ß-carboline alkaloid that was not reported previously.
Assuntos
Agaricales/química , Alcaloides/química , Carbolinas/química , Sequestradores de Radicais Livres/química , Alcaloides/isolamento & purificação , Carbolinas/isolamento & purificação , Sequestradores de Radicais Livres/isolamento & purificação , Hungria , Estrutura MolecularRESUMO
Acute total sleep deprivation (SD) impairs memory consolidation, attention, working memory and perception. Structural, electrophysiological and molecular experimental approaches provided evidences for the involvement of sleep in synaptic functions. Despite the wide scientific interest on the effects of sleep on the synapse, there is a lack of systematic investigation of sleep-related changes in the synaptic proteome. We isolated parietal cortical and thalamic synaptosomes of rats after 8h of total SD by gentle handling and 16h after the end of deprivation to investigate the short- and longer-term effects of SD on the synaptic proteome, respectively. The SD efficiency was verified by electrophysiology. Protein abundance alterations of the synaptosomes were analyzed by fluorescent two-dimensional differential gel electrophoresis and by tandem mass spectrometry. As several altered proteins were found to be involved in synaptic strength regulation, our data can support the synaptic homeostasis hypothesis function of sleep and highlight the long-term influence of SD after the recovery sleep period, mostly on cortical synapses. Furthermore, the large-scale and brain area-specific protein network change in the synapses may support both ideas of sleep-related synaptogenesis and molecular maintenance and reorganization in normal rat brain.