Figure 8

Inhibition of NF-κB activation in the ischemic brain by minocycline treatment in the wild type, but not in MCPIP1-deficient mice. A representative Western blot shows protein levels of p-65 phosphorylation. The phosphorylation of p-65 was significantly reduced at 24 h after MCAO in minocycline-pretreated wild type mice compared to that of the control. In MCPIP1-deficient mice, there was no significant difference in p-65 phosphorylation level between the minocycline-pretreated and control group without minocycline treatment. Densitometric analysis was used to quantify phospho-p-65 protein levels versus total p-65 in three independent Western blots, and the data are expressed as the normalized folds with respect to sham. Values represent mean ± SD. MCAO, middle cerebral artery occlusion; MCPIP1, monocyte chemotactic protein-induced protein 1.