title: Dexmedetomidine Attenuates Lipopolysaccharide Induced MCP-1 Expression in Primary Astrocyte.
abstract: Background. Neuroinflammation which presents as a possible mechanism of delirium is associated with MCP-1, an important proinflammatory factor which is expressed on astrocytes. It is known that dexmedetomidine (DEX) possesses potent anti-inflammatory properties. This study aimed to investigate the potential effects of DEX on the production of MCP-1 in lipopolysaccharide-stimulated astrocytes.Materials and Methods. Astrocytes were treated with LPS (10 ng/ml, 50 ng/ml, 100 ng/ml, and 1000 ng/ml), DEX (500 ng/mL), LPS (100 ng/ml), and DEX (10, 100, and 500 ng/mL) for a duration of three hours; expression levels of MCP-1 were measured by real-time PCR. The double immunofluorescence staining protocol was utilized to determine the expression ofα2-adrenoceptors (α2AR) and glial fibrillary acidic protein (GFAP) on astrocytes.Results. Expressions of MCP-1 mRNA in astrocytes were induced dose-dependently by LPS. Administration of DEX significantly inhibited the expression of MCP-1 mRNA (P< 0.001). Double immunofluorescence assay showed thatα2AR colocalize with GFAP, which indicates the expression ofα2-adrenoceptors in astrocytes.Conclusions. DEX is a potent suppressor of MCP-1 in astrocytes induced with lipopolysaccharide throughα2A-adrenergic receptors, which potentially explains its beneficial effects in the treatment of delirium by attenuating neuroinflammation.
authors.affiliation: Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Huan
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Jacques R J
authors.identifier: 0000-0003-3201-0994
authors.initials: JR
authors.lastname: Davis
authors.affiliation: Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Zhi-Lin
authors.identifier: 0000-0002-9179-1762
authors.initials: ZL
authors.lastname: Wu
authors.affiliation: Department of Anesthesiology, ICU and Pain Management, Benha University Hospital, Faculty of Medicine, Benha University, Benha, Egypt.
authors.forename: Amro
authors.initials: A
authors.lastname: Faez Abdelgawad
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis*; D020927:Dexmedetomidine / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects*; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000096:biosynthesis
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; C000614142:Gfap protein, rat; D005904:Glial Fibrillary Acidic Protein; D008070:Lipopolysaccharides; D018341:Receptors, Adrenergic, alpha-2; D020927:Dexmedetomidine