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. 2020 Sep 10;53:38. doi: 10.1186/s40659-020-00304-4

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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/. 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 in a credit line to the data.

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Fig. 1 — SNHG14 overexpression promotes apoptosis of OGD/R-induced HT22 cells. HT22 cell model was established by OGD/R treatment. Normal HT22 cells served as control. a QRT-PCR was performed to assess the expression of SNHG14 in the HT22 cells. HT22 cells were transfected with pcDNA3.1-SNHG14, pcDNA3.1-NC, si-SNHG14 or si-Ctrl. Then, the modified HT22 cells were subjected to OGD/R treatment. b QRT-PCR was performed to detect the expression of SNHG14 in the modified HT22 cells. c Flow cytometry was performed to explore the apoptosis of the modified HT22 cells. d The expression of caspase-3, cleaved-caspase-3, caspase-9 and cleaved-caspase-9 in the modified HT22 cells was examined by WB. (*P < 0.05, **P < 0.01, versus Control or Vector; ^#P < 0.05, ^##P < 0.01, versus si-Ctrl)