Figure 10.

Lipopolysaccharide (LPS)-induced activation of NF-κB canonical pathway was inhibited in toll-like receptor (TLR)-4^−/− and myeloid differentiation primary response (MyD)88^−/− mice and with transforming growth factor-β–activating kinase (TAK)-1 inhibition. A: LPS i.p. injections (0.1 mg/kg body weight) in TLR-4^−/− and MyD88^−/− mice did not induce inhibitory κ B (IκB)-α degradation (day 3) compared with TLR4^+/+ and MyD88^+/+ control (C) mice, respectively. Densitometry of IκB-α protein. B: Pretreatment with TAK-1 inhibitor (in; inh), oxyzeanol (Oxz; 5 mg/kg body weight), prevented the LPS-induced degradation of IκB-α expression (day 3) compared with vehicle- or LPS-treated mice. Densitometry of IκB-α protein levels. n = 3 experiments. ^∗∗P < 0.01 versus control; ^††P < 0.01 versus LPS.