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. 2016 May 23;6:33. doi: 10.1186/s13578-016-0099-1

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 6 — Exogenous H₂S inhibited activation of AMPK through ameliorating mitochondrial injury induced by oxidative stress. a The ATP level and the activities of the mitochondrial respiration chain complex II and III and IV were tested by kits. (*p < 0.05 vs control group. **p < 0.01 vs control group. ^#p < 0.05 vs HG + Pal group). b The whole ROS level was measured by DCFH (green fluorescence), and the mitochondrial ROS was measured by mito-SOX (red fluorescence). The mean fluorescence intensity was measured. There data were summarized from at least three different experiments. (**p < 0.01 vs control group. ***p < 0.001 vs control group. ^#p < 0.05 vs HG + Pal group. ^##p < 0.01 vs HG + Pal group. ^###p < 0.001 vs HG + Pal group). c The activity of CAT and SOD was detected with activity test kits. (*p < 0.05 vs control group. ^#p < 0.05 vs HG + Pal group. ^##p < 0.01 vs HG + Pal group)