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. 2002 May;50(5):658–664. doi: 10.1136/gut.50.5.658

Figure 4.

Figure 4

Characterisation of peroxisome proliferator activated receptor γ (PPARγ) ligand induced HT-29 cell death. Experiments were performed in the absence of fetal bovine serum. (A) Effects of 18 hours of treatment with 15-deoxy-δ12,14- prostaglandin J2 (15d-PGJ2 10 μM) or troglitazone (TGZ 20 μM) on the amount of fragmented DNA (n=6–8). **p<0.01 versus control. (B) Effect of a caspase inhibitor (CI), Z-Asp(OMe)-Glu(OMe)-Val-DL-Asp(OMe)-fmk (25 μM), on TGZ (30 μM) induced HT-29 cell death (n=6–8). HT-29 cells were preincubated with 25 μM CI for two hours and further incubated with 20 μM TGZ for 24 hours in the continued presence of the caspase inhibitor. p<0.01 TGZ versus CI/TGZ. (C) Effect of cycloheximide (CHX 25 μM) on TGZ (20 μM) induced HT-29 cell death (n=6–8). Cells were preincubated with 25 μM CHX for two hours and further incubated with 20 μM TGZ for 24 hours in the continued presence of CHX. p<0.01 TGZ versus CHX/TGZ.