Inhibition of NF-κB activation in the ischemic brain by EA treatment in the wild-type, but not in MCPIP1 knockout mice. Activation of NF-κB signaling pathway. A representative western blot shows protein levels of p65 phosphorylation. The phosphorylation of p65 was significantly reduced at 24 h after MCAO in EA-pretreated wild-type mice compared to that of control. In MCPIP1-deficient mice, there was no significant difference in p65 phosphorylation level between the EA-pretreated and the control group without EA treatment. Densitometric analysis was used to quantify phospho-p65 protein levels versus total p65 in three independent western blots and the data are expressed as the normalized folds with respect to sham. Values represent mean ± SD. EA, electroacupuncture; MCAO, middle cerebral artery occlusion; MCPIP1, monocyte chemotactic protein-induced protein 1; NF-κB, nuclear factor-kappa B; SD, standard deviation.