Opposite effects of anandamide and n‐arachidonoyl dopamine in the regulation of prostaglandin E2 and 8‐iso‐PGF2α formation in primary glial cells

@article{Navarrete2009OppositeEO,
  title={Opposite effects of anandamide and n‐arachidonoyl dopamine in the regulation of prostaglandin E2 and 8‐iso‐PGF2$\alpha$ formation in primary glial cells},
  author={Carmen M Navarrete and Bernd L Fiebich and Amaya Garc{\'i}a de Vinuesa and Sandra Hess and Antonio Carlos Pinheiro de Oliveira and Eduardo Candelario-Jalil and Francisco Javier Caballero and Marco A. Calzado and Eduardo Mu{\~n}oz},
  journal={Journal of Neurochemistry},
  year={2009},
  volume={109}
}
It is widely accepted that neuroinflammation is a key player in various pathological events associated with brain injury. More specifically, glial activation and the subsequent release of pro‐inflammatory cytokines, reactive oxygen species (ROS), and prostaglandins play a role of paramount importance in cerebral damage. In this study, we examined the role of two endocannabinoids, anandamide (AEA) and N‐arachidonoyldopamine (NADA) in the regulation of prostaglandin E2 (PGE2) synthesis in primary… 
N-Arachidonoyl Dopamine: A Novel Endocannabinoid and Endovanilloid with Widespread Physiological and Pharmacological Activities
TLDR
Findings provide strong evidence that NADA is an effective agent to manage neuroinflammatory diseases or pain and can be useful in designing novel therapeutic strategies.
N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1
TLDR
It is demonstrated that NADA potently decreases in vivo systemic inflammatory responses and levels of the coagulation intermediary plasminogen activator inhibitor 1 in three mouse models of inflammation and suggested that the endovanilloid system might be targeted therapeutically in acute inflammation.
The Endocannabinoid/Endovanilloid N-Arachidonoyl Dopamine (NADA) and Synthetic Cannabinoid WIN55,212-2 Abate the Inflammatory Activation of Human Endothelial Cells*
TLDR
It is demonstrated that the synthetic cannabinoid WIN55,212-2 and the eCB N-arachidonoyl dopamine (NADA) reduce EC inflammatory responses induced by bacterial lipopeptide, LPS, and TNFα, and may have important implications for a variety of acute inflammatory disorders that are characterized by EC activation.
Opposite Effects of Methanandamide on Lipopolysaccharide-Induced Prostaglandin E2 and F2α Synthesis in Uterine Explants from Pregnant Mice
TLDR
It is shown that anandamide (AEA) is involved in LPS-induced PG biosynthesis and the effect of exogenous AEA on different steps of PG metabolic pathway is observed, suggesting that AEA could be involved in the mechanisms implicated in L PS-induced ER.
Role of Endocannabinoids in Neuron-Glial Crosstalk
TLDR
Although eCBs are emerging as neurotransmitters responsible for the regu- lation of glia-neuron crosstalk in chronic pain, the precise mechanisms leading to eCB production, the origin and the time- course of e CB release, the eCB release switch from one cell type to the other and their movement or catabolism across the glial or neural cell membrane nevertheless still remain unknown.
Immunosuppressive and anti‐inflammatory effects of N‐acyl dopamines on Con A‐stimulated splenocytes of BALB/c mouse
TLDR
The findings suggest that N-acyl dopamines may express immuno-modulatory action through pathways involving CB1 and TRPV1 receptors in splenocytes through pathways involved in the regulation of inflammation and immunomodulation in BALB/c mice.
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