Fig. 7.

PPARα is downregulated and CHOP is visibly increased in individuals with HBV-related ALF. (A) Relative hepatic mRNA expression levels of PPARα and CHOP were measured by qRT-PCR in healthy controls (n=8), individuals with CHB (n=12) and individuals with ALF (n=12). (B) Protein levels of PPARα and CHOP were measured by western blotting. A representative blot from two samples of every group is shown. (C) Immunofluorescence staining for PPARα (green) and CHOP (red) in liver tissues from the patient groups. A representative experiment is shown. Original magnification 400×. (D) Schematic showing that in the progression of D-GalN/LPS-induced ALF in mice, mild ER stress is induced in the early phase of acute liver injury, which upregulates the expression of PPARα, but the severe ER stress is induced in the late phase of ALF, which downregulates the expression of PPARα. Decreased PPARα triggers CHOP activity, induces extensive hepatocyte apoptosis, and ultimately induces the development of ALF. Therefore, PPARα is a fulcrum in the regulation of ER stress-induced liver injury.