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. 2018 Jun 19;12:414. doi: 10.3389/fnins.2018.00414

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Copyright © 2018 Zheng, Shi, Liang, Xu, Li, Gao, Sun, Yu and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hyperglycemia suppressed sirt3 expression and aggravated cerebral injury after ICH. (A) Representative images of brain sections in each group. HE staining of ICH and the bleeding site (red circle). (B) Glucose levels of streptozotocin (STZ) treated and non-STZ-treated rats before and after experimental intracerebral hemorrhage (ICH), ^∗P < 0.05 versus non-STZ-treated group (n = 6 in each group). (C) Western blotting showed the sirt3 protein expression in HG and NG group on days 1, 3, and 5 after ICH, ^∗P < 0.05 (n = 6 in each group). HG, high blood glucose; NG, normal blood glucose. (D) The comparison of brain water content in HG and NG group on days 1, 3, and 5 after ICH, ^∗P < 0.05 (n = 6 in each group). (E) The comparison of neurologic deficit scores in HG and NG group on days 1, 3, and 5 after ICH, ^∗P < 0.05 (n = 9 in each group).