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. 2018 Oct 11;10(10):410. doi: 10.3390/toxins10100410

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Transient exposure to 20 mM urea induces persistent expression of inflammatory markers and MnTBAP reverses these. mRNA levels of NF-κB p65 subunit (A); VCAM1 (B); and MCP-1 (C) in HAEC exposed to 20 mM urea for 48 h or to 20 mM urea for 48 h followed by two days of subsequent incubation in media alone ± MnTBAP. Data are the mean ± S.E. from five independent experiments. * p < 0.05 compared to cells treated in the same conditions but not exposed to urea, # p < 0.05 cells not treated with the inhibitor compared to cells treated with MnTBAP.

Inline graphic — Transient exposure to 20 mM urea induces persistent expression of inflammatory markers and MnTBAP reverses these. mRNA levels of NF-κB p65 subunit (A); VCAM1 (B); and MCP-1 (C) in HAEC exposed to 20 mM urea for 48 h or to 20 mM urea for 48 h followed by two days of subsequent incubation in media alone ± MnTBAP. Data are the mean ± S.E. from five independent experiments. * p < 0.05 compared to cells treated in the same conditions but not exposed to urea, # p < 0.05 cells not treated with the inhibitor compared to cells treated with MnTBAP.