Figure 3.

TAZ exerted anti-inflammation and antioxidant functions by directly targeting Nrf2

(A and B) Regulation of TAZ activation on expression of Nrf2 mRNA and protein. N = 4. (C) TAZ boosted the transcriptional activity of Nrf2. After co-transfection with the TAZ overexpression plasmid and pARE-luc vector, followed by addition of LPS, luciferase activity was measured. N = 5. (D) Schematic showing the TAZ/TEAD binding site and mutation in the Nrf2 promoter region. (E) ChIP analysis revealed the binding enrichment of TAZ/TEAD to the Nrf2 promoter region. N = 3. (F) Luciferase analysis indicating the binding site of TAZ/TEAD to the Nrf2 promoter. N = 3. (G and H) Blockage of Nrf2 by ML385 resisted the restoration of TAZ on the production of IL-1β, IL-6, and TNF-α. N = 4. (I and J) Suppression of Nrf2 antagonized attenuation of TAZ on MDA and 8-OHdG levels. N = 4. (K and L) Impediment of Nrf2 counteracted the improvement of TAZ on intracellular ROS and O₂⁻. N = 3. (M–P) Blockage of Nrf2 antagonized rescue of TAZ on antioxidant enzyme activities, GSH content, and GSH/GSSG ratio. N = 4.