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. 2018 Apr 1;9(2):235–248. doi: 10.14336/AD.2017.0328

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Copyright: © 2018 Han et al.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 7. — Effects of TOPK overexpression, TOPK siRNA, the HDAC1/2 specific inhibitor FK228, and the broad-spectrum HDACi SAHA on microglia/macrophage M1/M2 polarization and cerebral injury in mice following 45 min ischemia/14 days reperfusion. (A) The western blotting verified the overexpression and knockdown of TOPK in ipsilateral brain tissue of mice intracerebroventricularly injected with TOPK overexpressing and siRNA4 letivirus. (B) Representative images of HE-stained sections (upper panels) and assessment of cerebral atrophy (lower panel). (C) Western blot (left) and corresponding quantitative analysis (right) of the expression of M1 markers (CD16 and iNOS) and M2 markers (CD206 and Arg1) in the ipsilateral brain of ischemic mice. *p < 0.05 versus sham, ^#p < 0.05 versus MCAO. (D) Immunofluorescence images stained for the M2 marker CD206 (red, first row) or M1 marker CD16 (red, third row), the microglia/macrophage marker Iba1 (green) and DAPI (blue), which showed the changes in CD206 and CD16 positive microglia/macrophage in the ipsilesional brain at 14 days following tMCAO (vehicle, TOPK overexpression, TOPK siRNA, TOPK siRNA+FK228 and TOPK siRNA +SAHA groups) or sham surgery (sham group). Images were taken from the red-boxed area in the brain slice of TTC staining. Scale bar: 20 μm. con, control letivirus. N=6. Statistics: Tukey’s honest significance test.