Figure 2.

TAZ inhibited the inflammatory response by enhancing antioxidant capacity

(A and B) Measurement of MDA and 8-OHdG levels after introduction of the TAZ overexpression plasmid and addition of LPS. N = 6. (C and D) Regulation of TAZ overexpression on intracellular ROS and O₂⁻ after exposure to LPS. N = 3. (E and F) Effects of TAZ overexpression on the activity of the antioxidant enzymes SOD, CAT, GPX, and GR in the context of LPS. N = 4. (G and H) GSH content and the GSH/GSSG ratio were determined after introduction of the TAZ overexpression plasmid and addition of LPS. N = 4. (I and J) Blockage of antioxidant enzymes and GSH synthesis by the corresponding inhibitors antagonized alleviation of TAZ on MDA and 8-OHdG levels. After introduction of the TAZ overexpression plasmid, MDA and 8-OHdG levels were analyzed in the presence or absence of the SOD inhibitor DDC, the CAT inhibitor 3AT, the GPX inhibitor MSA, the GR inhibitor BCNU, or the GSH synthesis inhibitor BSO in the context of LPS. N = 6. (K–M) Repression of antioxidant enzymes and GSH synthesis neutralized recovery of TAZ on the levels for IL-1β, IL-6, and TNF-α mRNA. N = 6. (N–P) Impediment of antioxidant enzymes and GSH synthesis counteracted rescue of TAZ on the release of IL-1β, IL-6 and TNF-α. N = 6. ∗p < 0.05 versus control in one-way ANOVA with Tukey’s post hoc test, #p < 0.05 versus LPS treatment in one-way ANOVA with Tukey’s post hoc test, &p < 0.05 versus transfection with the TAZ overexpression plasmid followed by addition of LPS in one-way ANOVA with Tukey’s post hoc test.