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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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HKL mediated the expression of sirt3 and its downstream signaling molecules after hyperglycemic ICH. (A) Sirt3 protein expression was significantly enhanced by HKL in a dose-dependent manner. ^#P < 0.05 versus ICH + vehicle group, ^∗P < 0.05 (n = 6 in each group). (B) NRF1 expression, ^∗P < 0.05 versus ICH + vehicle group (n = 6 in each group). (C) TFAM expression, ^∗P < 0.05 versus ICH + vehicle group (n = 6 in each group). (D) Ac-SOD2/SOD2 ratio (Ac-SOD2, acetylated SOD2), ^∗P < 0.05 versus ICH + vehicle group (n = 6 in each group). (E) Cleaved caspase3 expression, ^∗P < 0.05 versus ICH + vehicle group (n = 6 in each group). (F) Representative co-labeling cleaved-caspase3/NeuN images of ipsilateral basal ganglia. Quantification of cleaved caspase3-positive neurons (% = cleaved caspase3-positive neurons/total neurons), ^∗P and ^#P < 0.05 versus the rest groups (n = 6 in each group). Scale bars: 100 μm.