Modulation of Compound 48/80-induced RBL-2H3 degranulation.

<p>Compound 48/80 treatment of RBL- 2H3 cells induced a concentration dependent release of β-hexosaminidase. 30 minutes pre-incubation with 10 and 100 µM fexofenadine reduced β-hexosaminidase release in control cells and cells treated with 500 and 1000 µg Compound 48/80/ml (figure A). Carebastine pretreatment did not show an effect on Compound 48/80 stimulated RBL-2H3 cells (figure B). Results are a representative example of 3 independent experiments and expressed as mean ± SEM (4 wells per condition, *<i>P</i><0.05).</p

In vivo post stress fexofenadine treatment.

<p>The visceromotor response to distension was measured pre-WA and 24 and 48 hours post-WA in NH and MS rats. Fexofenadine or vehicle was administered 3 times between 24- and 48 hours measurements (cumulative dosages 18 and 1.8 mg/kg). Responses to distension are depicted as AUC (left side histograms) and per volume (right side line-diagrams, corresponding statistics in lower right side tables). NH rats did not become hypersensitive to distension and fexofenadine treatment did not change sensitivity levels (figures A and B). In MS rats WA induced enhanced sensitivity to distension in all 3 treatment groups (figures C, D and E). Treatment with 18 and 1.8 mg fexofenadine/kg (figure D and E respectively) but not vehicle alone (C) was able to reverse stress induced visceral hypersensitivity. All data are presented as mean ± SEM, all groups n = 8 or 9 rats, *<i>P</i><0.05 and **<i>P</i><0.01.</p

Relative colonic expression values for the <i>histamine H1 receptor</i> gene.

<p>H1R mRNA expression was evaluated relative to the housekeeping gene <i>Ppib</i> in colonic samples of NH and MS rats. Tissue was collected 7 days post vehicle treatment and distensions. There were no significant differences.</p