Fig. 5.

The H-PGDS-selective inhibitor HQL-79, but not the L-PGDS-selective inhibitor AT-56, attenuated LPS-induced PGD₂ production in BMDM. Primary cultured WT BMDM were treated with 1 μg/ml LPS for 16 hours in the presence of various concentrations of HQL-79 (A) or AT-56 (B). The concentrations of PGD₂ and PGE₂ were determined using LC-MS-MS. (A) HQL-79 concentration dependently (5, 20, and 100 μM) inhibited LPS-induced production of PGD₂, but not PGE₂, in BMDM (n = 6); (B) AT-56 did not affect LPS-induced either PGD₂ or PGE₂ production in BMDM (n = 3); (C) co-pretreatment (0.5 hour) of WT BMDM with HQL-79 (20 µM) and either DPI (0.5 µM) or PAO (0.1 µM) showed additive and selective inhibitory effects on LPS-induced production of PGD₂, but not PGE₂, in BMDM (n = 3).