Fig. 10.
Dexmedetomidine reverses lipopolysaccharide-induced NFκB–p65 phosphorylation in an α2 receptor–dependent manner. Four groups of randomly assigned cells (n = 4/group) were treated medium vehicle (control), lipopolysaccharide, lipopolysaccharide + dexmedetomidine, or yohimbine + lipopolysaccharide + dexmedetomidine. Twenty-four hours later, RAW 264.7 (A) and BV-2 (B) cell pellet were collected respectively, and the cell lysates were obtained for expression of NFκB–p65 phosphorylation by immunoblotting. The data are expressed as means ± SD relative to control and were analyzed by one-way ANOVA and Tukey post hoc test. *P < 0.05; **P < 0.01 for comparisons shown.

Dexmedetomidine reverses lipopolysaccharide-induced NFκB–p65 phosphorylation in an α2 receptor–dependent manner. Four groups of randomly assigned cells (n = 4/group) were treated medium vehicle (control), lipopolysaccharide, lipopolysaccharide + dexmedetomidine, or yohimbine + lipopolysaccharide + dexmedetomidine. Twenty-four hours later, RAW 264.7 (A) and BV-2 (B) cell pellet were collected respectively, and the cell lysates were obtained for expression of NFκB–p65 phosphorylation by immunoblotting. The data are expressed as means ± SD relative to control and were analyzed by one-way ANOVA and Tukey post hoc test. *P < 0.05; **P < 0.01 for comparisons shown.

Close Modal

or Create an Account

Close Modal
Close Modal