Figure 7.

TAZ repressed NF-κB by enhancing antioxidant capacity dependent on Nrf2

(A) Western blot analysis of IκBα, phosphorylated IκBα, and p65 expression after transfection with the TAZ overexpression plasmid, followed by addition of the corresponding inhibitor for antioxidant enzymes, GSH synthesis, and Nrf2. p-IκBα, phosphorylated IκBα. N = 3. (B) Visualization of nc p65 after introduction of the TAZ overexpression plasmid and EGFP-p65 vector, followed by nc staining with Hoechst 33342 in the presence or absence of different inhibitors or the NF-κB activator BA. N = 3. (C) Determination of NF-κB transcriptional activity after introduction of the TAZ overexpression plasmid and pNFκB-luc vector in the presence or absence of different inhibitors or the NF-κB activator BA. N = 5. (D) Effects of the NF-κB activator BA on expression of IκBα, phosphorylated IκBα, and p65 after introduction of the TAZ overexpression plasmid. N = 3. (E) Activation of NF-κB by BA resisted the recruitment of TAZ on the levels for IL-1β, IL-6, and TNF-α mRNA. N = 5. (F) Activation of NF-κB by BA counteracted the rescue of TAZ on the release of IL-1β, IL-6 and TNF-α. N = 5.