Alleviation of Microglial Activation Induced by p38 MAPK/MK2/PGE 2 Axis by Capsaicin: Potential Involvement of other than TRPV1 Mechanism/s

Exaggerated inflammatory responses in microglia represent one of the major risk factors for various central nervous system's (CNS) associated pathologies. Release of excessive inflammatory mediators such as prostaglandins and cytokines are the hallmark of hyper-activated microglia. Here we have...

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Veröffentlicht in:	Scientific reports 2017-03, Vol.7 (1), p.116
Hauptverfasser:	Bhatia, Harsharan S, Roelofs, Nora, Muñoz, Eduardo, Fiebich, Bernd L
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Capsaicin - pharmacology Cells, Cultured Cytokines - metabolism Dinoprostone - metabolism Gene Expression Regulation - drug effects Hippocampus - cytology Hippocampus - drug effects Hippocampus - metabolism Humans Intracellular Signaling Peptides and Proteins - metabolism MAP Kinase Signaling System - drug effects Mice Microglia - cytology Microglia - drug effects Microglia - metabolism Protein-Serine-Threonine Kinases - metabolism Rats TRPV Cation Channels - metabolism
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Zusammenfassung:	Exaggerated inflammatory responses in microglia represent one of the major risk factors for various central nervous system's (CNS) associated pathologies. Release of excessive inflammatory mediators such as prostaglandins and cytokines are the hallmark of hyper-activated microglia. Here we have investigated the hitherto unknown effects of capsaicin (cap) - a transient receptor potential vanilloid 1 (TRPV1) agonist- in murine primary microglia, organotypic hippocampal slice cultures (OHSCs) and human primary monocytes. Results demonstrate that cap (0.1-25 µM) significantly (p
ISSN:	2045-2322
DOI:	10.1038/s41598-017-00225-5