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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke

Fig. 6

Deficiency of ARRB2 restrained adrenergic-mediated inhibition of the phosphorylation activity of NF-κB signaling pathway. NA (100 μM) stimulation was applied to simulate the state of sympathetic pathway activation. a Representative western blot image showing the expression of NF-κB p65, IκBα, phosphor-IκBα, and ARRB2 in each group. b Densitometry analysis shown as graph bars for each protein expression normalized with β-actin. Increased expression of NF-κB p65 and phosphor-IκBα, and decreased expression of IκBα were detected in the LPS-stimulation group. Adrenergic-stimulation significantly inhibited LPS-induced NF-κB p65 and phosphor-IκBα expression. Meanwhile, increased expression of ARRB2 and IκBα was detected. Deficiency of ARRB2 significantly increased phosphor-IκBα and NF-κB p65 expression, and decreased IκBα expression in spite of adrenergic-stimulation. Each experiment was independently replicated three times. *P < 0.05 and **P < 0.01 by one-way ANOVA

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