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. 2020 Mar 6;20:73. doi: 10.1186/s12935-020-1152-z

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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. 1 — LPS-triggered production of proinflammatory cytokines in k562 cells. Cytokines and chemokines in LPS-treated k562 cells were detected using qPCR, ELISA, and WB. a Influence of LPS treatment on mRNA expressions of inflammatory cytokines in k562 cells determined via qPCR. b qPCR was performed to examine the mRNA expression of inflammatory cytokines after LPS treatment in k562 cells. In qPCR, gene expressionin each group was first normalized to the GAPDH gene, and then normalized to the data of the control group. c Influence of LPS treatment on the protein expressions of inflammatory cytokines in k562 cells determined via ELISA. d, e Influence of LPS treatment on protein levels of IL-1β, IL-6, and TNF-α in both k562 and KU812 cells determined via WB analyses. Data are expressed as mean ± standard deviation. *P < 0.05, **P < 0.01 relative to the control