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. 2007 Jul 26;406(Pt 1):175–183. doi: 10.1042/BJ20070089

Figure 4. Effects of arachidonic acid, 4β-PMA, PGF2α, NSAIDs and synthetic PPARα agonists with and without PKC inhibitors.

Figure 4

Bovine endometrial stromal cells were cultured for 6 h with or without additions, and PTGS2 was measured by immunoblotting. (a) Effects of 4β-PMA (2μM), PGF2α (3 μM) and RO318425 (RO; 500 nM). In the absence of the PPAR ligand, PTGS2 level was increased by 4β-PMA (P<0.001) and PGF2α (P<0.05), and the effect of 4β-PMA was blocked by RO318425 (P<0.005). Results were obtained from four experiments. (b) PTGS2 level was increased by arachidonic acid (AA; P<0.001), and the effect of arachidonic acid was blocked by RO318425 (P<0.001) and calphostin C (Cal; 500 nM). Results were obtained from six experiments. Neither RO318425 (Figure 4a) nor calphostin C (Figure 4b) affected PTGS2 when added alone. (c) Indomethacin and NS398 increased PTGS2 levels (P<0.001 in both cases). The effects of NSAIDs were blocked by RO318425. Results were obtained from five experiments. (d) The effects of the synthetic PPARα agonists WY14643 (200 μM) and ciprofibrate (200 μM) were blocked by RO318425 (500 nM). Results were obtained from three experiments.