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. 2017 Apr 21;7:1014. doi: 10.1038/s41598-017-00936-9

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© The Author(s) 2017

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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Expression of proteins in the PERK/Nrf2 pathway in RSC96 cells treated with TLN and exposed to high glucose. (A) High content analysis of p-PERK, Nrf2 and γGCS at 24 and 48 h. Images show immunostaining of RSC96 cells (10× magnification). (B–D) Fold changes of p-PERK, Nrf2 and γGCS levels relative to these after 25 mM glucose treatment. (E) Representative Western blots of GRP78, Keap1 and HO-1 in RSC96 cells 24 and 48 h. (F–H) Relative protein levels of GRP78, Keap1 and HO-1 against of β-actin. Data are represented as the means ± S.E.M. ^Δ P < 0.05, ^ΔΔ P < 0.01 vs. 25 mM glucose groups; ^# P < 0.05, ^## P < 0.01 vs. 150 mM glucose groups; ^* P < 0.05, ^** P < 0.01 vs. treated after 24 hours. Data were analyzed by One-way ANOVA followed by least significant difference or Tambane’s T2 analysis and Student’s unpaired t-test compared to 24 hours’ time point. (n = 4 per group).