ABSTRACT: There are multiple sources of reactive oxygen species (ROS) in the cell. As a major site of ROS production, mitochondria have drawn considerable interest because it was recently discovered that mitochondrial ROS (mtROS) directly stimulate the production of proinflammatory cytokines and pathological conditions as diverse as malignancies, autoimmune diseases, and ... Continue Reading
Inflammation
STUDY: Impaired NFAT and NFκB Activation are Involved in Suppression of CD40 Ligand Expression by Δ9-Tetrahydrocannabinol in Human CD4+ T cells
ABSTRACT: We have previously reported that Δ9-tetrahydrocannabinol (Δ9-THC), the main psychoactive cannabinoid in marijuana, suppresses CD40 ligand (CD40L) expression by activated mouse CD4+ T cells. CD40L is involved in pathogenesis of many autoimmune and inflammatory diseases. In the present study, we investigated the molecular mechanism of Δ9-THC-mediated suppression of ... Continue Reading
STUDY: Modulation of l-α-Lysophosphatidylinositol/ GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids*
ABSTRACT: GPR55 is activated by l-α-lysophosphatidylinositol (LPI) but also by certain cannabinoids. In this study, we investigated the GPR55 pharmacology of various cannabinoids, including analogues of the CB1 receptor antagonist Rimonabant®, CB2receptor agonists, and Cannabis sativa constituents. To test ERK1/2 phosphorylation, a primary downstream signaling pathway that ... Continue Reading
STUDY: Role of TNF-alpha during central sensitization in preclinical studies
ABSTRACT: Tumor necrosis factor-alpha (TNF-α) is a principal mediator in pro-inflammatory processes that involve necrosis, apoptosis and proliferation. Experimental and clinical evidence demonstrate that peripheral nerve injury results in activation and morphological changes of microglial cells in the spinal cord. These adjustments occur in order to initiate an inflammatory ... Continue Reading
STUDY: The fatty acid amide hydrolase inhibitor URB597 exerts anti-inflammatory effects in hippocampus of aged rats and restores an age-related deficit in long-term potentiation
ABSTRACT: Background Several factors contribute to the deterioration in synaptic plasticity which accompanies age and one of these is neuroinflammation. This is characterized by increased microglial activation associated with increased production of proinflammatory cytokines like interleukin-1β (IL-1β). In aged rats these neuroinflammatory changes are associated with a ... Continue Reading