Further supporting these findings, we showed that oral treatment with TQ blocked the increased IκBα and p65 phosphorylation in the stomach of HCl/EtOH-treated mice (Fig. 4d, left panel) and also reduced the phosphorylation of MKK4 and c-Jun (components of the MAPK/AP-1 pathway) and p65, IκBα, and AKT (components of the NF-κB pathway) in the LPS/D-GalN-induced hepatitis mouse model (Fig. 4d, right panel). Here, NFKB1 is linked to hepatitis A virus infection.