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. 2019 Jul 22;17:81. doi: 10.1186/s12964-019-0396-5

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — Suppression of pro-inflammatory macrophages by TNTL improved the endothelial condition in retina. a. showed that TNTL treatment could significantly reduce the infiltration and residence of F4/80+ macrophages; b. showed that supernatant (SN) from TNTL-treated pro-inflammatory BMDMs had minimal effect on the cell viability of retinal endothelial cells (RECs); c. showed that SN from TNTL-treated pro-inflammatory BMDMs failed in inducing RECs migration; d. showed that SN from TNTL-treated pro-inflammatory BMDMs induced loss of monolayer integrity formed by RECs; e. showed that SN from TNTL-treated pro-inflammatory BMDMs led to the leakage of FITC-Dextran through RECs monolayers. *p < 0.05, **p < 0.01, ***p < 0.001 when compared with model group