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. 2018 Jul 10;8:10394. doi: 10.1038/s41598-018-28500-z

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© The Author(s) 2018

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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Treatment of NFκ-B inhibitors reduce HIV-1 replication in U1 cells due to BaP exposure. U1 cells were concomitantly treated with BaP (1 µM) and NFκ-B inhibitors, IKK-16 (400 nM) (A), and SC-514 (10 µM) (B) for 3 days. After the treatment, supernatants were collected to determine the viral load using the p24 ELISA assay. HIV-1 replication due to BaP (1 µM) exposure was significantly rescued by NFκ-B inhibitors, IKK-16 (400 nM) and SC-514 (10 µM). *Represents p ≤ 0.05 compared with the control group while ^## represents p ≤ 0.005 compared to the BaP-treated groups. Western blots were run using the nuclear fraction proteins obtained from the BaP-exposed cells treated with IKK-16 (C) SC-524 (D) or siRNA CYP1A1 (E) to determine the expression of NFκ-B p65 subunits. The blots indicate that treatment with both the NFκ-B inhibitors and CYP1A1 siRNA reduced the expression of NFκ-B p65 in the nuclear fraction protein of the BaP-treated cells compared to the control. The blots presented are representative of at least three different experiments.