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. 2023 Jul 17;19(7):e1011506. doi: 10.1371/journal.ppat.1011506

Fig 4. Antiviral effects of the four compounds are NRF2-independent.

Fig 4

hiPSC-derived wild-type or NRF2-/- vascular ECs were pretreated with the compounds (SEL, 1 μM; 4OI, 100 μM; BARD, 0.1 μM; SFN, 10 μM) for 12 h, infected with IAV PR8M (MOI = 1) for 2 h, and then incubated in fresh buffer containing the compounds for 22 h. A. NFE2L2 mRNA (RT-qPCR). B. Viral titers in cell culture supernatants (foci-forming assay, FFU/mL). C, D. IFIT1 and CXCL10 mRNA (RT-qPCR). E. Expression of HMOX1, SLC7A11, AKR1B10, GCLM, and KEAP1 mRNAs (RT-qPCR, internal control HPRT1 mRNA), heat map based on log2 fold change (as indicated in the color legend) with respect to expression in wild-type uninfected cells. Column graphs of these data are shown in S3 Fig for additional clarity. F-H, Knocking down KEAP1 expression reduces viral titers, but does not affect the antiviral effect of the compounds. F, Expression of KEAP1 mRNA (RT-qPCR). G, Expression of viral HA mRNA (RT-qPCR). H, Viral titers (foci-forming assay, FFU/ml). n = 3, means ±SEM. One-way ANOVA with Tukey’s post-hoc test. * ≤0.05, ** ≤0.01, *** ≤0.001, **** ≤0.0001.