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. 2019 Nov 8;9:16296. doi: 10.1038/s41598-019-52494-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Inhibition of mitochondrial ROS generation improves the ICH-induced neurological deficits. (A–D) N-acetylcysteine (NAC), apocynin or mitoQ10 was intraperitoneally injected at a dose of 5, 20 or 10 mg/kg immediately after ICH surgery in WT and RNF34 transgenic mice. Summarized data of neurological deficits as assessed by rotarod test (A), pole test (B), beam-crossing task (C), and traction test (D). (E,F) The oxidative stress indicators GSH (E) and MDA (F) concentrations in brain tissues were determined. n = 6 per group. **P < 0.01 vs. WT sham; ^#P < 0.05, ^##P < 0.01 vs. WT ICH; &&P < 0.01 vs TG ICH, n = 20/group.