1,721,059 research outputs found
THE P2Y-LIKE PURINERGIC/CYSTEINYL- LEUKOTRIENE RECEPTOR GPR17 AS A TARGET FOR BRAIN REPAIR IN NEURODEGENERATIVE DISEASES
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Purinergic signalling in inflammation of the central nervous system
No full textInflammation is the most fundamental body reaction to noxious stimuli. No vascularized tissue, organ or apparatus is free from this response. Several mediators of inflammation, originating from outside (exogenous) or inside (endogenous) the body, are known. Among the endogenous factors, extracellular nucleotides and nucleosides are attracting interest for their ubiquity and striking ability to modulate diverse immune responses. Until recently, it was doubted that the central nervous system (CNS), reportedly an 'immunoprivileged organ', could be the site of immune reactions. Nowadays, it is acknowledged that inflammation and immunity have a key role in a vast range of CNS diseases. Likewise, it is clear that purinergic signalling profoundly affects neuroinflammation. Here, we provide a brief update of the state of the art in this expanding field
Short-term TNF-alpha treatment induced A2B adenosine receptor desensitization in human astroglial cells
No full textLong-term glial cell treatment with the proinflammatory cytokine TNF-alpha has been demonstrated to increase the functional responsiveness of A 2B adenosine receptors (A2B ARs), which in turn synergize with the cytokine inducing chronic astrogliosis. In the present study, we investigated the short-term effects of TNF-alpha on A2B AR functional responses in human astroglial cells (ADF), thus simulating the acute phase of cerebral damage which is characterized by both cytokine and adenosine high level release. Short-term TNF-alpha cell treatment caused A2B AR phosphorylation inducing, in turn, impairment in A2B AR-G protein coupling and cAMP production. These effects occurred in a time-dependent manner with a maximum following 3-h cell exposure. Moreover, we showed PKC intracellular kinase is mainly involved in the TNF-alpha-mediated regulation of A2B AR functional responses. The results may indicate the A 2B AR functional impairment as a cell defense mechanism to counteract the A2B receptor-mediated effects during the acute phase of brain damage, underlying A2B AR as a target to modulate early inflammatory responses. © 2007 Wiley-Liss, Inc
PHARMACOLOGICAL CHARACTERIZATION OF P2X AND P2Y PURINOCEPTORS IN RAT BLADDER SMOOTH-MUSCLE AND EPITHELIUM
No full textAntitumor effects of cannabidiol , a nonpsychoative cannabinoid, on Human glioma cell lines
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