Alleviation of Microglial Activation Induced by p38 MAPK/MK2/PGE₂ Axis by Capsaicin: Potential Involvement of other than TRPV1 Mechanism/s.

ABSTRACT: 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 < 0.05) inhibited the release of prostaglandin E₂ (PGE₂)_, 8-iso-PGF_2α, and differentially regulated the levels of cytokines (TNF-α, IL-6 & IL-1β). Pharmacological blockade (v

SUBMITTER: Bhatia HS 

PROVIDER: S-EPMC5428011 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature