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. 2014 Mar;88(5):2810–2820. doi: 10.1128/JVI.03205-13

FIG 3.

FIG 3

PRRSV induces PGE2 production through COX-1. (A) PAMs were pretreated with COX-1 inhibitor sc-560 (2.5 nM, 10 nM) or COX-2 inhibitor celecoxib (10 nM, 40 nM) for 1 h and then infected with HP-PRRSV strain JXnw06 (MOI, 2). Cell supernatants were harvested at 24 hpi and analyzed for PGE2 production using ELISA. (B) PAMs were pretreated with COX-1 inhibitor sc-560 at different dosages (1 nM, 10 nM, and 50 nM) for 1 h and then infected with HP-PRRSV strain JXnw06 (MOI, 2) in the absence or presence of sc-560. PGE2 production in cell supernatants was detected at 24 hpi by ELISA. (C) Intracellular PRRSV RNA was evaluated at 24 hpi using quantitative real-time PCR. “P” represents PRRSV infection. Data are means ± SEMs from at least three independent experiments. Differences were evaluated by Student's t test. (*, P < 0.05; **, P < 0.01; ns, not significant).