sr-144528 has been researched along with Intracranial-Hemorrhages* in 2 studies
2 other study(ies) available for sr-144528 and Intracranial-Hemorrhages
Article | Year |
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A selective CB2R agonist (JWH133) restores neuronal circuit after Germinal Matrix Hemorrhage in the preterm via CX3CR1
Microglia play dual roles after germinal matrix hemorrhage, and the neurotrophic phenotype maybe neuroprotective. However, the phenotype transformation and the way by which neuron-microglia dialogue remain unclear. We raise the hypothesis that a cannabinoid receptor2 agonist (JWH133) accelerates the CX3CR1 Topics: Animals; Animals, Newborn; Brain Injuries; Brain-Derived Neurotrophic Factor; Camphanes; Cannabinoids; CX3C Chemokine Receptor 1; Disease Models, Animal; Female; In Vitro Techniques; Intracranial Hemorrhages; Male; Microglia; Nerve Tissue Proteins; Pregnancy; Pyrazoles; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB2; Receptors, Chemokine; RNA, Small Interfering; Up-Regulation | 2017 |
Cannabinoid CB2 receptor stimulation attenuates brain edema and neurological deficits in a germinal matrix hemorrhage rat model.
Germinal matrix hemorrhage (GMH) is one of the most common and devastating cerebrovascular events that affect premature infants, resulting in a significant socioeconomic burden. However, GMH has been largely unpreventable, and clinical treatments are mostly inadequate. In the present study, we tested the hypothesis that JWH133, a selective CB2 receptor agonist, could attenuate brain injury and neurological deficits in a clostridial collagenase VII induced GMH model in seven-day-old (P7) S-D rat pups. Up to 1h post-injury, the administration of JWH133 (1mg/kg, intraperitoneal injection) significantly attenuated brain edema at 24h post-GMH, which was reversed by a selective CB2R antagonist, SR144528 (3mg/kg, intraperitoneal injection). Long-term brain morphology and neurofunctional outcomes were also improved. In contrast, JWH133 did not have a noticeable effect on the hematoma volume during the acute phase. These data also showed that microglia activation and inflammatory cytokine (TNF-α) release were significantly inhibited by JWH133 after GMH. This current study suggests a potential clinical utility for CB2R agonists as a potential therapy to reduce neurological injury and improve patient outcomes after GMH. Topics: Acute Disease; Animals; Brain; Brain Edema; Camphanes; Cannabinoid Receptor Agonists; Cannabinoid Receptor Antagonists; Cannabinoids; Chronic Disease; Disease Models, Animal; Female; Intracranial Hemorrhages; Male; Microglia; Movement; Neuroprotective Agents; Pyrazoles; Random Allocation; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB2; Tumor Necrosis Factor-alpha | 2015 |