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. 2017 Aug 31;7:10270. doi: 10.1038/s41598-017-10619-0

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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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miR-96 inhibits hippocampus Atg7 and Atg16L1 expression in SE rats. (A) The cell type specificity of Atg7 was performed with fluorescent immunolabeling (FITC-labeled, green). The nucleus was stained by DAPI (blue). Scale bar = 50 μm. The percent of Atg7 positive cells was analyzed (n = 5; **p < 0.01, compared with the ctrl group; ^##p < 0.01, compared with the SE-miR-NC group). (B) The cell type specificity of Atg16L1 was performed with fluorescent immunolabeling (FITC-labeled, green). The nucleus was stained by DAPI (blue). Scale bar = 50 μm. The percent of Atg16L1 positive cells was analyzed (n = 5; **p < 0.01, compared with the ctrl group; ^##p < 0.01, compared with the SE-miR-NC group). (C) Western blotting analysis of Atg7 and Atg16L1 expression in the hippocampus of SE rats. Equal levels of protein samples (20 μg) were loaded, andβ-actin served as a loading control. The relative optical density were analyzed and represented as the mean ± SD (n = 3; **p < 0.01, compared with the ctrl group; ^##p < 0.01, compared with the SE-miR-NC group).