Figure 3

Reduction in infarct size and improvement of neurological function by minocycline treatment in the wild type, but not in MCPIP1-deficient mice. The brain infarct size was assessed 48 h after MCAO. (A) Infarct images obtained by TTC staining at 48 h after MCAO. The normal tissue was stained deep red and the infarct was stained milky. (B) Brain infarcts were quantified as percentage area of ischemic hemisphere. The infarct size of minocycline-pretreated wild type mice was significantly reduced compared to that of the control. There was no significant difference in brain infarct size between the minocycline-pretreated and control in MCPIP1-deficient mice. (C) Brain water content as a measure of brain edema of the ischemic hemisphere. The brain edema was significantly reduced at 48 h after MCAO in minocycline-pretreated wild type mice compared to that of the control group. In the MCPIP1-deficient mice, there was no significant difference in brain water content between minocycline-pretreated and control group without minocycline treatment. (D) Neurological function assessment was performed 24 h after MCAO. The neurological scores of minocycline-pretreated wild type mice were significantly improved compared to that of the control. In MCPIP1-deficient mice, there was no significant difference in neurological deficits between minocycline-pretreated and control group. Values represent mean ± SD, *P < 0.05, n = 10 mice per group. MCAO, middle cerebral artery occlusion; MCPIP1, monocyte chemotactic protein-induced protein 1; TTC, 2,3,5-triphenyltetrazolium chloride.