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. 2020 Nov 22;17:350. doi: 10.1186/s12974-020-02022-w

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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 — Inhibitory effect of K284-6111 on Aβ-induced neuroinflammation in BV-2 cells. BV-2 cells were treated with Aβ (5 μM) and K284-6111 (0.5, 1, and 2 μM). a The inhibitory effect of K284-6111 on nitric oxide production was determined using a nitric oxide assay kit in BV-2 cells. b Expression of iNOS, COX-2, and IBA-1 was detected by Western blot. c The mRNA expression level of pro-inflammatory cytokines (Tnf, Il1b, and Il6) and M1 microglia phenotype marker (Cd86) were assessed by qRT-PCR. (D) The production levels of TNF-α, IL-1β, and IL-6 were assessed using the specific ELISA kits