sr-144528 and Intracranial-Hemorrhages

sr-144528 has been researched along with Intracranial-Hemorrhages* in 2 studies

Other Studies

2 other study(ies) available for sr-144528 and Intracranial-Hemorrhages

ArticleYear
A selective CB2R agonist (JWH133) restores neuronal circuit after Germinal Matrix Hemorrhage in the preterm via CX3CR1
    Neuropharmacology, 2017, Volume: 119

    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.
    Brain research, 2015, Mar-30, Volume: 1602

    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