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. 2021 Jan 6;16:6. doi: 10.1186/s13018-020-02041-6

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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/. 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 — LncRNA LEF-AS1 was upregulated in the SCI model in vivo and in vitro. a BBB scores were measured in sham and SCI groups. b Relative expression of lncRNA LEF-AS2 in sham and SCI groups. c Relative expression of lncRNA LEF-AS2 in control and LPS-treated microglia cells. d Cell viability in control and LPS-treated microglia cells measured by CCK-8 assay. e Apoptosis ratio in control and LPS-treated microglia cells measured by Annexin V/FITC apoptosis assay. f Western blot assay to measure the protein expression of apoptotic markers (Bax, Bcl-2, and cleaved-caspase-3). g Inflammatory cytokines (TNF-α and IL-6) expression levels in control and LPS-treated microglia cells (P < 0.05)