Fig. 3.
Dexmedetomidine prevents lipopolysaccharide-induced peripheral inflammation in an α2 receptor-dependent manner. Six groups of randomly assigned mice (n = 8/group) were administered saline vehicle (control), lipopolysaccharide, lipopolysaccharide + dexmedetomidine, atipamezole + lipopolysaccharide + dexmedetomidine, yohimbine + lipopolysaccharide + dexmedetomidine, or prazosin + lipopolysaccharide + dexmedetomidine. Six hours after lipopolysaccharide, the mice were euthanized, and the blood was harvested and assayed by enzyme-linked immunosorbent assay for circulating interleukin (IL)–1β. The data are expressed as means ± SD and analyzed by one-way ANOVA and Tukey post hoc test. ****P < 0.0001 for comparisons shown.

Dexmedetomidine prevents lipopolysaccharide-induced peripheral inflammation in an α2 receptor-dependent manner. Six groups of randomly assigned mice (n = 8/group) were administered saline vehicle (control), lipopolysaccharide, lipopolysaccharide + dexmedetomidine, atipamezole + lipopolysaccharide + dexmedetomidine, yohimbine + lipopolysaccharide + dexmedetomidine, or prazosin + lipopolysaccharide + dexmedetomidine. Six hours after lipopolysaccharide, the mice were euthanized, and the blood was harvested and assayed by enzyme-linked immunosorbent assay for circulating interleukin (IL)–1β. The data are expressed as means ± SD and analyzed by one-way ANOVA and Tukey post hoc test. ****P < 0.0001 for comparisons shown.

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