This effect does not seem to involve acetylcholine-stimulated nit

This effect does not seem to involve acetylcholine-stimulated nitric oxide release.

Copyright (C) 2008 S. Karger JQ1 cell line AG, Basel.”
“Microglial cell activation and migration play an important role in neuroinflammation propagation. While it is known that the lipid transmitter palmitoylethanolamide (PEA) regulates microglial migration by interacting with a cannabinoid-like receptor, the production and inactivation of this lipid by microglia has never been addressed directly. Here we show that the mouse microglial cell line BV-2 produces and hydrolyzes PEA. The carbamate compound URB602 inhibits PEA hydrolysis in BV-2 cell homogenates and increases PEA levels in intact cells, whereas the FAAH inhibitor URB597 and serine-hydrolase inhibitor MAFP do not affect PEA levels

in intact cells. This unique pharmacological profile of inhibitors on PEA hydrolysis suggests the involvement of a previously undescribed enzyme that degrades PEA. This enzyme expressed by microglia constitutes a promising target for controlling the propagation of neuroinflammation. Published by Elsevier Ltd.”
“The activity of NADPH oxidase (NOX) is blocked by nitric oxide (NO). Hydrogen sulfide (H2S) Crenolanib manufacturer is also produced by blood vessels. It is reasonable to suggest that H2S may have similar actions to NO on NOX. In order to test this hypothesis, the effect of sodium hydrosulfide (NaHS) on O-2(-) formation, the expression of NOX-1 (a catalytic subunit of NOX) and Rac(1) activity (essential for full NOX activity) in isolated vascular smooth muscle cells (hVSMCs) was investigated. hVSMCs were incubated with the thromboxane A(2) analogue U46619 +/- NaHS for 1 or 16 h, and O-2(-) formation, NOX-1 expression Roflumilast and Rac(1) activity were assessed. The

possible interaction between H2S and NO was also studied by using an NO synthase inhibitor, L-NAME, and an NO donor, DETA-NONOate. The role of K-ATP channels was studied by using glibenclamide. NaHS inhibited O-2(-) formation following incubation of 1 h (IC 50, 30 nM) and 16 h (IC 50, 20 nM), blocked NOX-1 expression and inhibited Rac(1) activity. These inhibitory effects of NaHS were mediated by the cAMP-protein-kinase-A axis. Exogenous H2S prevents NOX-driven intravascular oxidative stress through an a priori inhibition of Rac(1) and downregulation of NOX-1 protein expression, an effect mediated by activation of the adenylylcyclase-cAMP-protein-kinase-G system by H2S. Copyright (C) 2008 S. Karger AG, Basel.”
“Cannabinoid agonists regulate NO and cyclic AMP production in N18TG2 neuroblastoma cells, leading to the hypothesis that neuronal cyclic GMP production could be regulated by CB1 cannabinoid receptors. NO (nitric oxide)- sensitive guanylyl cyclase (GC) is a heterodimeric cytosolic protein that mediates the down-stream effects of NO.

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