Peroxisome proliferator-activated receptor γ ligands suppress liver carcinogenesis induced by diethylnitrosamine in rats

Figure 1 Experimental design for evaluation of chemoprevention efficacy of PPARγ ligands against liver carcinogenesis. A: In the short-term study of rGST P-positive foci, groups of male Wistar rats were fed experimental diets containing 0 or 200 or 1000 ppm of PPARγ ligands from 1 wk prior to exposure to DEN at 20 mg/kg bm until the termination. B: For liver tumor study, groups of animals were given the basal diet or experi-mental diet containing 200-ppm Pio continuously from 1 wk prior to exposure of animals to DEN, IP, at 1to 6 experimental weeks at 20 mg/kg bm until the termination.

Figure 2 Dose-dependent suppression of the formation of rGST P-positive foci by rosiglitazone. As clearly demonstrated, Rosi suppressed the formation of rGST P-positive foci in a dose-dependent manner within the range of 0.88-500 ppm in diet (^aP < 0.05, ^bP < 0.01).

Figure 3 Expression of PPARγ mRNA in liver tumors. Lanes 1 and 4: normal liver tissues; lanes 2, 3, 5, and 6: liver tumor tissues; lane 7: water.