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. 2020 Jul 20;18:100. doi: 10.1186/s12951-020-00656-9

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 4 — The mechanism behind the LDEVs effect on gastric cancer cells. a KEGG pathway analysis of SGC-7901 cells after LDEVs treatment for 6 h and b 12 h. The highest KEGG pathways were labeled by red line respectively. c RT-PCR assay the relative expression of GADD45A in AGS, BGC-823, and SGC-7901 cells treated with LDEVs; d Western blot analysis of GADD45α protein expression in three gastric cancer cells; e Flow cytometry assay the intracellular ROS levels using DCFH-DA; f Cell viability of control group, LDEVs group, NAC + LDEVs group, and NAC groups respectively (*p < 0.05; **p < 0.01, ***p < 0.001, ****p < 0.0001)