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. 2017 Feb 13;15(4):1682–1692. doi: 10.3892/mmr.2017.6195

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Copyright: © Wu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 6. — LXA₄-induced HO-1 expression was dependent on formation of the Nrf2/ARE complex. (A) HK-2 cells were transfected with M739, E1, dnNrf2, then treated with LXA₄ followed by exposure to H/R injury. Fold induction of luciferase activity of the HO-1 promoter was determined using reporter gene transfection assays. Data are presented as the mean ± standard deviation of 5 independent experiments. *P<0.05 vs. untreated control group. (B) Nuclear extracts of the cells were subjected to electrophoretic mobility shift assay with biotin-labeled double-stranded oligonucleotide probe of ARE. Supershift assay was conducted using the Nrf2 antibody. (C) Binding activity of Nrf2 to E1 was assessed using a chromatin immunoprecipitation assay in cells subjected to H/R injury, LXA₄ or H/R injury and LXA₄. HO-1, heme oxygenase-1; E1, mouse HO-1 promoter construct; M739, mutated mouse HO-1 promoter construct; H/R, hypoxia/reoxygenation; LXA₄, lipoxin A₄; dnNrf, dominant negative nuclear factor E2-related factor 2; ARE, antioxidant responsive element.