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. 2017 Nov 24;7:16226. doi: 10.1038/s41598-017-16373-7

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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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NGR1 inhibited OGD/R-induced stimulation of the ER stress and CaMKII pathway via PLC. (A,B) Western blotting analysis of ER stress and CaMKII pathway-related proteins. (C–I) When cells were exposed to NGR1 or U73122, there was less expression of p-PERK, p-IRE1, CHOP, p-CaMKII, p-P38, and p-JNK and more expression of BCL-2, but in the OGD/R + NGR1 + m-3M3FBS group, higher expression of p-PERK, p-IRE1, CHOP, p-CaMKII, p-P38, and p-JNK and lower expression of BCL-2 were detected. M-3M3FBS treatment could induce higher activation of ER stress and CaMKII than that in the OGD/R group. Original image of the cropped blots shown in Supplementary Figure S4. *p < 0.05 compared with the OGD/R groups, ^# p < 0.05 compared with the OGD/R + NGR1 groups, n = 5, data presented as mean ± SD.