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. 2020 Mar 4;32:101485. doi: 10.1016/j.redox.2020.101485

Fig. 3.

Fig. 3

BC-1901S increases NRF2-dependent gene transcription and decreases inflammation. A) RT-qPCR of GPx2 and HO-1 in Beas-2B cells treated with BC-1901S at 0, 0.1, 1, and 10 μM. Fold change (RQ) is normalized to endogenous GAPDH expression. Data and mean ± SD of 3 independent experiments. B) Beas-2B cells were transfected with an ARE-reporter (pGL4.37[luc2P/ARE/Hygro]) vector and treated with BC-1901S at various doses. Luminescence signals were collected and quantified. Data and mean ± SD of 3 independent experiments. C) NRF2, HO-1, GPx-1/2, and β-Actin immunoblots after NRF2 dsiRNA knockdown with or without BC-1901S treatment. D, E) PBMCs were treated with LPS or LPS and BC-1901S at various doses for 18h. Cell culture supernatants were then assayed for TNF (D) and IL-1β (E) using ELISA. Data and mean ± SD of 3 independent experiments. F) Immunoblot of NRF2 in MLE-12 after treatment with BC-1901S at indicated time points. G) MLE were treated with LPS or LPS and BC-1901S at various doses for 18h. Cell culture supernatants were then assayed for IL-6 using ELISA. Data and mean ± SD of 3 independent experiments. P < 0.05, *; P < 0.01, **; P < 0.001, ***; P < 0.0001, ****; by one-way ANOVA with adjusted P-value for multiple comparisons (Dunnett's) compared to “0”.