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. 2018 Aug 1;19:144. doi: 10.1186/s12931-018-0852-6

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© The Author(s). 2018

Open Access This 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. 7 — Effect of HO-1 byproducts on silica-induced pERK and HO-1 upregulation in RAW264.7 and 16HBE cells. Immunoblotting analysis showed that HO-1 byproducts, bilirubin and CO, suppress silica-induced ERK activation and subsequent HO-1 upregulation in (a) RAW264.7 cells and (b) 16HBE cells. Cells were pretreated with bilirubin or RuCO (CO releasing molecule) 1 h before silica exposure at the indicated concentrations and incubated as described in Fig. 4. Representative immunoblot images from three independent experiments are shown. Densitometric analysis of band intensity representing the mean ± SD level of pERK to ERK or HO-1 to actin from three independent experiments. ^# P < 0.05; ^## P < 0.01 vs silica only