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. 2020 Feb 14;10:2696. doi: 10.1038/s41598-020-59665-1

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© The Author(s) 2020

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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Ocellatin-K1(1–16) and Ocellatin-K1(1–21) prevented the LPS-induced NF-kB activation in living microglia. CHME3 human microglial cells expressing the biosensor of NF-kB pathway inhibitor were incubated with 100 μM Ocellatin-K1(1–16) or Ocellatin-K1(1–21) and challenged with 1 μg/mL LPS. Microglia were incubated only with Ocellatin-K1(1–16) and Ocellatin-K1(1–21) and compared with saline control group. Time-lapse fluorescence intensities for the NF-kB pathway inhibitor biosensor are shown (n = 17–19 cells pooled across two different experiments). The results are expressed as mean ± SEM. ^#p < 0.01 vs. LPS group; *p < 0.001 vs. CT not treated with LPS employing one-way ANOVA with Bonferroni post-test. Abbreviations: CT: control; LPS: lipopolysaccharide.