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. 2016 Feb 9;13:33. doi: 10.1186/s12974-016-0501-2

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© Liao et al. 2016

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 — Role of Oxidative-ER stress in cocaine-mediated up-regulation of TLR2 and microglial activation in BV2 cells. a, b Effect of pharmacological inhibitor of ER-stress 4-PBA on cocaine-mediated up-regulation of ATF4 and TLR2 proteins in BV2 cells. c Effect of 4-PBA on cocaine-mediated induction of TLR2, TNFα, IL-6, and MCP-1 mRNAs. Relative levels of TLR2, TNFα, IL-6, and MCP-1 mRNAs were analyzed by qPCR using 18S rRNA as an internal control. d Effects of 4-PBA on cocaine-mediated induction of TNFα and MCP-1 proteins assessed by ELISA. e 4-PBA did not ameliorate cocaine-mediated induction of ROS generation. f, g Effects of APO (NADPH oxidase inhibitor) and PBN (ROS scavenger) on cocaine-mediated up-regulation of ATF4 protein in BV2 cells. All data are presented as mean ± SD of three individual experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs control group. ^# p < 0.05, ^## p < 0.01 vs cocaine group (Student’s t test)