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. 2018 May 29;8:8346. doi: 10.1038/s41598-018-26421-5

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© The Author(s) 2018

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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The expression of MALAT1, MyD88, IRAK1 and TRAF6 in an in vitro model of DM-I/R. The rat primary microglia and microglia line HAPI were cultured to establish the cell model of DM-I/R with high glucose (HG) and hypoxia-reoxygenation (H/R). The cells were divided into 4 groups: LG-control (low glucose treatment, 5.5 mM), LG-H/R (LG and H/R treatment), HG-control (HG treatment, 30 mM), HG-H/R (HG and H/R treatment). (A) The expression of MALAT1. (B) Representative Western blot analysis of MyD88, IRAK1, TRAF6 protein. The relative expressions of (C) MyD88, (D) IRAK1, (E) TRAF6 protein were measured. ^*P < 0.01 vs. LG-control; ^#P < 0.01 vs. LG-H/R.