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https://www.selleckchem.com/products/gkt137831.html Background Clinical studies have shown that dexmedetomidine ameliorates cognitive decline in both the postoperative and critical care settings. This study determined the mechanism(s) for the benefit provided by dexmedetomidine in a medical illness in mice induced by lipopolysaccharide. Methods Cognitive decline, peripheral and hippocampal inflammation, blood-brain barrier permeability, and inflammation resolution were assessed in male mice. Dexmedetomidine was administered in the presence of lipopolysaccharide and in combination with blockers. Cultured macrophages (RAW 264.7; BV-2) were exposed to lipopolysaccharide ± dexmedetomidine ± yohimbine; tumor necrosis factor α release into the medium and monocyte NFκB activity was determined. Results In vivo, lipopolysaccharide-induced cognitive decline and inflammation (mean ± SD) were reversed by dexmedetomidine (freezing time, 55.68 ± 12.31 vs. 35.40 ± 17.66%, P = 0.0286, n = 14; plasma interleukin [IL]-1β 30.53 ± 9.53 vs. 75.68 ± 11.04 pg/ml, P less then 0.000cal studies suggest that the cognitive benefit provided by dexmedetomidine in mice administered lipopolysaccharide is mediated through α2 adrenoceptor-mediated anti-inflammatory pathways. WHAT WE ALREADY KNOW ABOUT THIS TOPIC Administration of lipopolysaccharide to young and middle-aged mice is associated with neuroinflammation and cognitive impairmentDexmedetomidine has been shown to decrease neuroinflammation in mice WHAT THIS ARTICLE TELLS US THAT IS NEW Administration of dexmedetomidine to mice treated with lipopolysaccharide decreased neuroinflammation and cognitive impairment in both young and aged miceThe effects of dexmedetomidine on neuroinflammation and cognitive impairment in mice treated with lipopolysaccharide are likely mediated by α2 adrenoceptor-mediated anti-inflammatory pathways.Purpose Valproic acid (VPA) is not only an antiepileptic drug but also a mood stabilizer for patients with bipolar dis

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