{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Martinez-Torres AM"],"funding":["Consejo Nacional de Humanidades, Ciencias y Tecnologías","Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México"],"pagination":["e70385"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12005396"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(4)"],"pubmed_abstract":["<h4>Background</h4>Intracerebral hemorrhage (ICH) is a leading cause of death and disability worldwide. Following the initial mechanical injury caused by hematoma expansion, a secondary injury occurs, characterized by the production of reactive oxygen species (ROS) generated by NOX-2 and neuroinflammation, which is exacerbated by the upregulation of the NLRP3 inflammasome. These conditions collectively aggravate brain damage. The endocannabinoid system (ECS), through the activation of the cannabinoid receptors, has demonstrated neuroprotective properties in various models of brain injury. However, the role of the ECS during ICH remains poorly understood, particularly regarding the action of the CB1 receptor in the activation of NOX-2 and the inflammasome. The present study investigates the"],"journal":["CNS neuroscience & therapeutics"],"pubmed_title":["Cannabinoid Receptors Reduced Early Brain Damage by Regulating NOX-2 and the NLRP3 Inflammasome in an Animal Model of Intracerebral Hemorrhage."],"pmcid":["PMC12005396"],"funding_grant_id":["IN216422","285184","IN224425"],"pubmed_authors":["Moran J","Martinez-Torres AM","Ramirez-Celis C"],"additional_accession":[]},"is_claimable":false,"name":"Cannabinoid Receptors Reduced Early Brain Damage by Regulating NOX-2 and the NLRP3 Inflammasome in an Animal Model of Intracerebral Hemorrhage.","description":"<h4>Background</h4>Intracerebral hemorrhage (ICH) is a leading cause of death and disability worldwide. Following the initial mechanical injury caused by hematoma expansion, a secondary injury occurs, characterized by the production of reactive oxygen species (ROS) generated by NOX-2 and neuroinflammation, which is exacerbated by the upregulation of the NLRP3 inflammasome. These conditions collectively aggravate brain damage. The endocannabinoid system (ECS), through the activation of the cannabinoid receptors, has demonstrated neuroprotective properties in various models of brain injury. However, the role of the ECS during ICH remains poorly understood, particularly regarding the action of the CB1 receptor in the activation of NOX-2 and the inflammasome. The present study investigates the","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2025-07-12T03:04:15.935Z","creation":"2025-07-12T03:04:15.935Z"},"accession":"S-EPMC12005396","cross_references":{"pubmed":["40245261"],"doi":["10.1111/cns.70385"]}}