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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAn2gOGvpRzZZGW5CjJMlzvtoUjppVVT2ILP_-7jXxaSg#_3 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAn2gOGvpRzZZGW5CjJMlzvtoUjppVVT2ILP_-7jXxaSg#_2 http://www.w3.org/ns/prov#value A COX-2-selective inhibitor, NS-398 (10 µM), was used to determine whether COX-2 was responsible for the observed increases in PGE2 synthesis by CSE-treated fibroblasts (62). Two different strains of human lung fibroblasts were pretreated with NS-398 for 1 h before treatment with 1% CSE for 24 h, and supernatants were analyzed for PGE2. As shown in Fig. 2, the fibroblast strains incubated with 1% CSE had a three- to fourfold induction in PGE2 synthesis over basal levels after 24 h, depending on the strain. 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