Fig. 8
From: β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke
Deficiency of ARRB2 significantly reverses adrenergic-stimulated monocyte dysfunction. The levels of cytokine release were detected by ELISA. LPS induced high release of IL-6 (a), TNF-α (b), IL-1β (c), and IL-8 (d). Adrenergic-stimulation significantly inhibited LPS-induced pro-inflammatory cytokine release including IL-6 (a), TNF-α (b), IL-1β (c), and IL-8 (d). However, deficiency of ARRB2 substantially reversed the adrenergic suppression in cytokine release by elevating IL-6 (a), TNF-α (b), IL-1β (c), and IL-8 (d) levels. Each experiment was independently replicated three times. *P < 0.05 and **P < 0.01 by one-way ANOVA