Fig. 5.
Schematic model for time-course changes in hepatic gene expressions of key factors during steatohepatitis and fibrosis progression in the stroke-prone, spontaneously hypertensive 5/Dmcr rat (SHRSP5/Dmcr) given the HFC-diet treatment. The current SHRSP5/Dmcr rat model appeared to show rather dynamic interplays and changes in the state of liver biochemical balances as shown by initial TNF-α and NF-κB hepatic inflammatory reactions in conjunction with pro-fibrogenic TGF-β1 responses that led to the progression of liver disease to extensive liver fibrosis, as indicated by the up-regulation of PDGF-B, α-SMA, and α1 type I collagen, the eventual down-regulation of proteins associated with PPARs and AMPKα, and down-regulation of DGAT1 and DGAT2 mRNA