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

  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},

Cytosolic phospholipase A2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway

The results in this study demonstrated the role of cPLA2 in microglial activation with metabolic links to oxidative and inflammatory responses, and this was in part regulated by the AA metabolic pathways, namely the LOXs.

CB2 Receptor Activation Ameliorates the Proinflammatory Activity in Acute Lung Injury Induced by Paraquat

It is suggested that activating CB2 receptor exerted protective activity against PQ-induced ALI, and it potentially contributed to the suppression of the activation of MAPKs and NF-κB pathways.

Anti-Inflammatory Effects by Pharmacological Inhibition or Knockdown of Fatty Acid Amide Hydrolase in BV2 Microglial Cells

Although inhibition and knockdown of FAAH have potent anti-inflammatory effects and possibly lead to the dynamic change of microglial gene regulation, the underlying mechanisms remain to be elucidated.

Modulation of breast cancer cell viability by a cannabinoid receptor 2 agonist, JWH-015, is calcium dependent

The results of this work characterize the actions of a CB2-selective agonist on breast cancer cells in a syngeneic murine model representing how a clinical presentation of cancer progression and metastasis may be significantly modulated by a G-protein-coupled receptor.

Non‐psychotropic Cannabis sativa L. phytocomplex modulates microglial inflammatory response through CB2 receptors‐, endocannabinoids‐, and NF‐κB‐mediated signaling

The data suggest that C. sativa phytocomplex and its multitarget mechanism could represent a novel therapeutic strategy for neuroinflammatory‐related diseases.

Inflammation and Nitro-oxidative Stress as Drivers of Endocannabinoid System Aberrations in Mood Disorders and Schizophrenia

It is suggested that cannabidiol and dimethyl fumarate may have therapeutic potential for major depressive disorder, bipolar disorder and schizophrenia.

Role of G Protein-Coupled Receptors in Microglial Activation: Implication in Parkinson’s Disease

The implication of microglial GPCRs-regulated neuroinflammation to the pathophysiology of PD and their potential to become a new expectation for clinical therapeutics are expounded.



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.

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.