Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Figure 1 Histological studies of rat livers in normal control, NAFLD and RGZ-treated NAFLD groups (x 400). Liver tissue sections were stained with HE, A: Normal control group; B: NAFLD group; C: RGZ-treated NAFLD group. Liver tissue sections were stained with oil red O, D: normal control group; E: NAFLD group; F: RGZ-treated NAFLD group. Liver tissue sections were stained with Masson’s trichrome, G: Normal control group; H: NAFLD group; I: RGZ-treated NAFLD group. Liver tissue sections were stained with immunohistochemistry for IL-18, J: Normal control group; K: NAFLD group; L: RGZ-treated NAFLD group. Liver tissue sections were stained with immunohistochemistry for caspase-1, M: Normal control group; N: NAFLD group; O: RGZ-treated NAFLD group. Histological changes in fatty liver disease and IL-18- or caspase-1-positive staining cells were rarely detectable in the control group. NAFLD rat liver showed steatosis and moderate inflammatory changes, fat droplet accumulation, mild fibrosis, strong IL-18- and caspase-1-positive staining. A significant improvement of steatosis, inflammation, fibrosis, and IL-18 and caspase-1 staining was observed in liver of the RGZ-treated NAFLD group.

Figure 2 RT-PCR analysis of mRNA expression of IL-18 (A) and caspase-1 (B) in liver tissues of the three groups. The histograms show the ratio of target gene expression to β-actin. Data are presented as mean ± SE from six independent experiments in the control group and eleven in the NAFLD and RGZ-treated NAFLD groups. ^aP < 0.05 vs control group, ^cP < 0.05 vs NAFLD group.