Dexmedetomidine Attenuates Lipopolysaccharide Induced MCP-1 Expression in Primary Astrocyte

Abstract

<i>Background</i>. 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. <i>Materials and Methods</i>. 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 of <i>α</i>2-adrenoceptors (<i>α</i>2AR) and glial fibrillary acidic protein (GFAP) on astrocytes. <i>Results</i>. Expressions of MCP-1 mRNA in astrocytes were induced dose-dependently by LPS. Administration of DEX significantly inhibited the expression of MCP-1 mRNA (<i>P</i> < 0.001). Double immunofluorescence assay showed that <i>α</i>2AR colocalize with GFAP, which indicates the expression of <i>α</i>2-adrenoceptors in astrocytes. <i>Conclusions</i>. DEX is a potent suppressor of MCP-1 in astrocytes induced with lipopolysaccharide through <i>α</i>₂A-adrenergic receptors, which potentially explains its beneficial effects in the treatment of delirium by attenuating neuroinflammation.