Figure 4

Reduction in infarct size and improvement of neurological function by 2-h post-treatment of minocycline on stroke in the wild type, but not in MCPIP1-deficient mice. (A) The results showed that the infarct size of minocycline-treated wild type mice was significantly reduced compared to that of the control (40.3% ± 6.1% versus 23.3% ± 4.7%, respectively; values represent mean ± SD, *P < 0.05, n = 10 mice per group). MCPIP1-deficient mice failed to evoke minocycline treatment-induced neuroprotection compared with that of control MCPIP1 knockout group without minocycline treatment (55.1% ± 4.9% versus 52.8% ± 5.3%). There was no significant difference in brain infarct size between minocycline-treated and control in MCPIP1 knockout mice. (B) The neurological functions of mice were determined, and the results showed that the neurological scores of minocycline-treated 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-treated and control group without minocycline treatment. MCPIP1, monocyte chemotactic protein-induced protein 1.