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. 2020 Apr 22;469(1):41–51. doi: 10.1007/s11010-020-03726-6

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — DEX upregulated the expression of SNHG16 and BDNF, and inhibited the expression of miR-10b-5p. The expression of SNHG16 (a), miR-10b-5p (b) and BDNF mRNA (c) in the brain tissues of MCAO rats was detected by qPCR after DEX treatment at different concentrations, and the protein expression of BDNF in the tissues was detected by Western blot (d). An in vitro OGD neuron injury model was established. After DEX treatment at different concentrations, the expression of SNHG16 (e), miR-10b-5p (f) and BDNF mRNA (g) in neurons was detected by qPCR, and the protein expression of BDNF in neurons was detected by Western blot (h). *, **, *** represents P < 0.05, P < 0.01 and P < 0.001 compared with the Sham group or Control group. ^#, ^##, ^### indicates that compared with MCAO group or OGD group, P < 0.05, P < 0.01 and P < 0.001