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. 2017 Oct 16;7:13248. doi: 10.1038/s41598-017-13251-0

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© The Author(s) 2017

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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Protective effects of NaHS on mitochondrial biogenesis was blocked by LY-294002, Compound C and CamKKβ in IR cellular model. (a) The mitochondrial complexes were determined by Western blot. Expression of OXPHOS components was decreased in the PA-induced IR model and reversed by NaHS treatment. Inhibitors of CamKK2, AMPK and PI3K blocked the effects mediated by NaHS. *p < 0.05, **p < 0.01, ***p < 0.001, ^#p < 0.05, ^##p < 0.01, ⁺p < 0.05, ⁺⁺p < 0.01, ^^p < 0.01. Data are shown as the mean ± SD. (b) ATP production in the IR group was decreased, but upregulated in response to NaHS treatment. Inhibitors of CamKK2, AMPK and PI3K blocked this upregulation. *p < 0.05, **p < 0.05, ***p < 0.001. Data are shown as the mean ± SD.