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. 2018 Aug 6;18:192. doi: 10.1186/s12886-018-0864-5

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — HMGB1 mediates intermittent high glucose-induced autophagy. DAPI was used to stain the nuclei. a-b: Immunohistochemistry showed that the normal glucose ARPE-19 cells were mainly expressed as nuclear localization of HMGB1. However, in ARPE-19 cells treated with intermittent high glucose, the proportion of HMGB1 in the cytoplasm was increased. c-d: EP could inhibite intermittent high glucose-induced LC3-II expression. e: EP could increase the expression of p62 protein under conditions of intermittent high glucose. f: Loss of HMGB1 under intermittent high glucose condition resulted in dramatic significantly reduction in proliferative activity than intermittent high glucose and normal glucose(*p < 0.05 vs. control, ^#p < 0.05 vs. HG)