u-0126 has been researched along with Nerve-Degeneration* in 3 studies
3 other study(ies) available for u-0126 and Nerve-Degeneration
| Article | Year |
|---|---|
TRPC6-mediated ERK1/2 phosphorylation prevents dentate granule cell degeneration via inhibiting mitochondrial elongation.
Topics: Animals; Butadienes; Disease Models, Animal; Dynamins; Enzyme Inhibitors; Male; Mitochondria; Mitochondrial Dynamics; Mitogen-Activated Protein Kinase 12; Muscarinic Agonists; Nerve Degeneration; Nerve Tissue Proteins; Neurons; Nitriles; Phosphorylation; Pilocarpine; Rats; Rats, Sprague-Dawley; RNA, Small Interfering; Signal Transduction; Status Epilepticus; TRPC Cation Channels | 2017 |
Beneficial Effect of Astragaloside on Alzheimer's Disease Condition Using Cultured Primary Cortical Cells Under β-amyloid Exposure.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Apoptosis; Butadienes; Caspase 3; Cells, Cultured; Cerebral Cortex; Extracellular Signal-Regulated MAP Kinases; Male; Memory Disorders; Mitochondria; Nerve Degeneration; Neurons; Nitriles; Phosphorylation; Proto-Oncogene Proteins c-akt; Rats, Sprague-Dawley; Saponins; Synapses; tau Proteins | 2016 |
Cannabinoid receptor 2 attenuates microglial accumulation and brain injury following germinal matrix hemorrhage via ERK dephosphorylation in vivo and in vitro.
Microglia accumulation plays detrimental roles in the pathology of germinal matrix hemorrhage (GMH) in the immature preterm brain. However, the underlying mechanisms remain poorly defined. Here, we investigated the effects of a cannabinoid receptor 2 (CB2R) agonist on microglia proliferation and the possible involvement of the mitogen-activated protein kinase (MAPK) family pathway in a collagenase-induced GMH rat model and in thrombin-induced rat microglia cells. We demonstrated that activation of CB2R played a key role in attenuating brain edema, neuronal degeneration, microglial accumulation and the phosphorylated extracellular signal-regulated kinase (p-ERK) protein level 24 h following GMH. In vitro, Western blot analysis and immunostaining indicated that ERK and P38 phosphorylation levels in microglia stimulated by thrombin were decreased after JWH-133 (CB2R selective agonist) treatment in a concentration-dependent manner. Microglia proliferation (EDU + microglia) and inflammatory and oxidative stress responses were attenuated by UO126 (ERK pathway inhibitor) 24 h after thrombin stimulation, an activity that was prevented by AM630 (CB2R selective antagonist). Overall, these findings suggest that activation of the endocannabinoid system might attenuate inflammation-induced secondary brain injury after GMH in rats by reducing microglia accumulation through a mechanism involving ERK dephosphorylation. Enhancing CB2R activation is a potential treatment to slow down the course of GMH in preterm newborns. Topics: Animals; Brain; Brain Edema; Butadienes; Cannabinoids; Cell Proliferation; Cells, Cultured; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Indoles; Intracranial Hemorrhages; Male; Microglia; Nerve Degeneration; Neuroimmunomodulation; Nitriles; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Protein Kinase Inhibitors; Random Allocation; Receptor, Cannabinoid, CB2; Thrombin | 2015 |