Fig. 2: Cardiac glycosides digoxin and lanatoside C modify inflammation-dependent transcriptional responses in pericytes.

a–l Conditioned media from pericytes after 24 h of vehicle, digoxin (blue bars) or lanatoside C (red bars) (125 nM points selected from concentration curves in Fig. S2) pre-treatment prior to stimulation with IL1β (0.05 ng mL⁻¹) for 24 h (n = 3, cases used: E206, E213, E214). m–p Pericytes pre-treated with digoxin (100 nM) or lanatoside C (1 µM) for 24 h were treated with IL-1β (0.05 ng mL⁻¹) for 1 h, and stained for CEBPδ or NFκB, (representative images (m and o, scale = 100 µm), (n) quantification of CEBPδ percent positive cells, and (p) percent NFκB nuclear translocation were compared to control conditions. Two-way ANOVA with Tukey’s multiple comparison test, mean ± SEM.***p < 0.001, **p < 0.01, *p < 0.05, (n = 3, cases used: E204, E206, E208). q Pericytes were pre-treated with vehicle or lanatoside C (1 µM) for 24 h, then treated with vehicle or IL-1β (0.05 ng mL⁻¹) for 30 min. Lysates (500 µg per sample) were analysed using the human NFκB array kit. Average intensity values from duplicate spots were normalised to the average intensity of the reference spots on each blot (n = 1, case used: E213). r Select targets from NFκB profiler presented as fold change in intensity from vehicle.