Involvement of ERK1/2, cPLA2 and NF-κB in microglia suppression by cannabinoid receptor agonists and antagonists.

@article{Ribeiro2013InvolvementOE,
  title={Involvement of ERK1/2, cPLA2 and NF-$\kappa$B in microglia suppression by cannabinoid receptor agonists and antagonists.},
  author={Rachel Ribeiro and Jie Wen and Shihe Li and Yumin Zhang},
  journal={Prostaglandins \& other lipid mediators},
  year={2013},
  volume={100-101},
  pages={
          1-14
        }
}
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43 Citations

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References

SHOWING 1-10 OF 58 REFERENCES

Cannabinoid receptor type 2 activation induces a microglial anti-inflammatory phenotype and reduces migration via MKP induction and ERK dephosphorylation

The results suggest that the reduction of pro-inflammatory factors and microglial migration via MKP-3 induction is part of the mechanism of action of CBR2 agonists, and may have clinical implications for further drug development.

The central cannabinoid receptor (CB1) mediates inhibition of nitric oxide production by rat microglial cells.

Results indicate a functional linkage between the CB1 receptor and cannabinoid-mediated inhibition of NO production by rat microglial cells.

Cannabinoids Δ9-Tetrahydrocannabinol and Cannabidiol Differentially Inhibit the Lipopolysaccharide-activated NF-κB and Interferon-β/STAT Proinflammatory Pathways in BV-2 Microglial Cells*

Observations show that CBD and THC vary in their effects on the anti-inflammatory pathways, including the NF-κB and IFNβ-dependent pathways.

Anandamide enhances IL‐10 production in activated microglia by targeting CB2 receptors: Roles of ERK1/2, JNK, and NF‐κB

By altering the cytokine network, AEA could indirectly modify the type of immune responses within the central nervous system (CNS) and pharmacological modulation of AEA uptake and degradation might be a useful tool for treating neuroinflammatory diseases.

Arachidonylcyclopropylamide increases microglial cell migration through cannabinoid CB2 and abnormal-cannabidiol-sensitive receptors.

A role for CB2 receptors in anandamide signalling pathways involved in the regulation of IL-12 and IL-23 in microglial cells.

Cannabinoid Type 2 Receptor Activation Downregulates Stroke-Induced Classic and Alternative Brain Macrophage/Microglial Activation Concomitant to Neuroprotection

The inhibitory effect of CB2R on the activation of different subpopulations of microglia/macrophages may account for the protective effect of the selectiveCB2R agonist JWH-133 after stroke.

Synthetic cannabinoid WIN55,212‐2 inhibits generation of inflammatory mediators by IL‐1β‐stimulated human astrocytes

Findings indicate that WIN55,212‐2 inhibits the production of inflammatory mediators by IL‐1β‐stimulated human astrocytes and suggest that comparable agents may have therapeutic potential for the management of brain inflammation.

Nonpsychotropic Cannabinoid Receptors Regulate Microglial Cell Migration

This study identifies a cannabinoid signaling system regulating microglial cell migration and proposes that cannabinol and cannabidiol are promising nonpsychotropic therapeutics to prevent the recruitment of these cells at neuroinflammatory lesion sites.

Cannabinoids ablate release of TNFα in rat microglial cells stimulated with lypopolysaccharide

The data indicate that both synthetic and endogenous cannabinoids inhibit LPS‐induced release of TNFα from microglial cells, providing evidence suggestive of the existence of yet unidentified cannabinoid receptor(s) in brain microglia.
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