{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Longhitano L"],"funding":["PON AIM R&I","Piano di Incentivi per la ricercar di Ateneo","Piano di Incentivi per la ricercar di Ateneo 2020/2022 Linea di intervento 2 (G.L.V)"],"pagination":["1682"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9495359"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(9)"],"pubmed_abstract":["Cerebrovascular ischemia is a common clinical disease encompassing a series of complex pathophysiological processes in which oxidative stress plays a major role. The present study aimed to evaluate the effects of Dexmedetomidine, Clonidine, and Propofol in a model of hypoxia/reoxygenation injury. Microglial cells were exposed to 1%hypoxia for 3 h and reoxygenated for 3 h, and oxidative stress was measured by ROS formation and the expression of inflammatory process genes. Mitochondrial dysfunction was assessed by membrane potential maintenance and the levels of various metabolites involved in energetic metabolism. The results showed that Propofol and α2-agonists attenuate the formation of ROS during hypoxia and after reoxygenation. Furthermore, the α2-agonists treatment restored membrane po"],"journal":["Antioxidants (Basel, Switzerland)"],"pubmed_title":["Propofol and α2-Agonists Attenuate Microglia Activation and Restore Mitochondrial Function in an In Vitro Model of Microglia Hypoxia/Reoxygenation."],"pmcid":["PMC9495359"],"funding_grant_id":["2020/2022","PON AIM R&I 2014-2020-E66C18001240007","2014-2020-E66C18001240007"],"pubmed_authors":["Garofalo E","Astuto M","Bruni A","Amorini AM","Volti GL","Sanfilippo F","Lazzarino G","Distefano A","Murabito P","Buscema G","Longhitano L","Tibullo D","Nicolosi A"],"additional_accession":[]},"is_claimable":false,"name":"Propofol and α2-Agonists Attenuate Microglia Activation and Restore Mitochondrial Function in an In Vitro Model of Microglia Hypoxia/Reoxygenation.","description":"Cerebrovascular ischemia is a common clinical disease encompassing a series of complex pathophysiological processes in which oxidative stress plays a major role. The present study aimed to evaluate the effects of Dexmedetomidine, Clonidine, and Propofol in a model of hypoxia/reoxygenation injury. Microglial cells were exposed to 1%hypoxia for 3 h and reoxygenated for 3 h, and oxidative stress was measured by ROS formation and the expression of inflammatory process genes. Mitochondrial dysfunction was assessed by membrane potential maintenance and the levels of various metabolites involved in energetic metabolism. The results showed that Propofol and α2-agonists attenuate the formation of ROS during hypoxia and after reoxygenation. Furthermore, the α2-agonists treatment restored membrane po","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-04-08T12:01:47.616Z","creation":"2024-11-13T18:59:40.971Z"},"accession":"S-EPMC9495359","cross_references":{"pubmed":["36139756"],"doi":["10.3390/antiox11091682"]}}