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Matches in Nanopublications for { ?s ?p "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. However, cells treated with both CSE and NS-398 had significantly decreased PGE2 levels relative to fibroblasts treated with CSE alone, supporting the idea that the elevated PGE2 levels are a result of COX-2 activity. " ?g. }

• _2 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. However, cells treated with both CSE and NS-398 had significantly decreased PGE2 levels relative to fibroblasts treated with CSE alone, supporting the idea that the elevated PGE2 levels are a result of COX-2 activity. " provenance.
• _4 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. However, cells treated with both CSE and NS-398 had significantly decreased PGE2 levels relative to fibroblasts treated with CSE alone, supporting the idea that the elevated PGE2 levels are a result of COX-2 activity. " provenance.
• _2 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. However, cells treated with both CSE and NS-398 had significantly decreased PGE2 levels relative to fibroblasts treated with CSE alone, supporting the idea that the elevated PGE2 levels are a result of COX-2 activity. " provenance.
• _4 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. However, cells treated with both CSE and NS-398 had significantly decreased PGE2 levels relative to fibroblasts treated with CSE alone, supporting the idea that the elevated PGE2 levels are a result of COX-2 activity. " provenance.