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Effects of non-steroidal anti-inflammatory drugs on prostaglandin E2 production by cyclooxygenase-2 from endogenous and exogenous arachidonic acid in rat peritoneal macrophages stimulated with lipopolysaccharide.

Abstract

Lipopolysaccharide (LPS) stimulated prostaglandin E2 (PGE2) formation and induction of cyclooxygenase-2 (COX-2) expression without changing the levels of COX-1 protein in rat peritoneal macrophages. Non-steroidal anti-inflammatory drugs (NSAIDs) (nimesulide, indomethacin and ibuprofen) strongly inhibited LPS-stimulated PGE2 production without any effect on COX-2 protein expression, suggesting that NSAIDs are active in inhibiting the ability of COX-2 to convert arachidonic acid (AA) endogenously released in response to LPS stimulation. Exogenous AA can be converted to PGE2 by both COX isoforms even in LPS-stimulated macrophages. NSAIDs inhibited PGE2 production from exogenous AA mediated by both COX-1 and COX-2. However, the two isoforms interacted differentially with different NSAIDs. Furthermore, NSAIDs were distinctly more active in inhibiting PGE2 production from endogenous AA than that from exogenous AA. These data suggest that PGE2 production through COX-2 from exogenous AA may not be subject to the same regulatory processes as that from endogenous AA and the two metabolic processes may be differentially sensitive to different NSAIDs.

Authors+Show Affiliations

Osaka Research Laboratory, Sawai Pharmaceutical Co. Ltd., Japan.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9014225

Citation

Nakatsugi, S, et al. "Effects of Non-steroidal Anti-inflammatory Drugs On Prostaglandin E2 Production By Cyclooxygenase-2 From Endogenous and Exogenous Arachidonic Acid in Rat Peritoneal Macrophages Stimulated With Lipopolysaccharide." Prostaglandins, Leukotrienes, and Essential Fatty Acids, vol. 55, no. 6, 1996, pp. 451-7.
Nakatsugi S, Sugimoto N, Furukawa M. Effects of non-steroidal anti-inflammatory drugs on prostaglandin E2 production by cyclooxygenase-2 from endogenous and exogenous arachidonic acid in rat peritoneal macrophages stimulated with lipopolysaccharide. Prostaglandins Leukot Essent Fatty Acids. 1996;55(6):451-7.
Nakatsugi, S., Sugimoto, N., & Furukawa, M. (1996). Effects of non-steroidal anti-inflammatory drugs on prostaglandin E2 production by cyclooxygenase-2 from endogenous and exogenous arachidonic acid in rat peritoneal macrophages stimulated with lipopolysaccharide. Prostaglandins, Leukotrienes, and Essential Fatty Acids, 55(6), 451-7.
Nakatsugi S, Sugimoto N, Furukawa M. Effects of Non-steroidal Anti-inflammatory Drugs On Prostaglandin E2 Production By Cyclooxygenase-2 From Endogenous and Exogenous Arachidonic Acid in Rat Peritoneal Macrophages Stimulated With Lipopolysaccharide. Prostaglandins Leukot Essent Fatty Acids. 1996;55(6):451-7. PubMed PMID: 9014225.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of non-steroidal anti-inflammatory drugs on prostaglandin E2 production by cyclooxygenase-2 from endogenous and exogenous arachidonic acid in rat peritoneal macrophages stimulated with lipopolysaccharide. AU - Nakatsugi,S, AU - Sugimoto,N, AU - Furukawa,M, PY - 1996/12/1/pubmed PY - 1996/12/1/medline PY - 1996/12/1/entrez SP - 451 EP - 7 JF - Prostaglandins, leukotrienes, and essential fatty acids JO - Prostaglandins Leukot. Essent. Fatty Acids VL - 55 IS - 6 N2 - Lipopolysaccharide (LPS) stimulated prostaglandin E2 (PGE2) formation and induction of cyclooxygenase-2 (COX-2) expression without changing the levels of COX-1 protein in rat peritoneal macrophages. Non-steroidal anti-inflammatory drugs (NSAIDs) (nimesulide, indomethacin and ibuprofen) strongly inhibited LPS-stimulated PGE2 production without any effect on COX-2 protein expression, suggesting that NSAIDs are active in inhibiting the ability of COX-2 to convert arachidonic acid (AA) endogenously released in response to LPS stimulation. Exogenous AA can be converted to PGE2 by both COX isoforms even in LPS-stimulated macrophages. NSAIDs inhibited PGE2 production from exogenous AA mediated by both COX-1 and COX-2. However, the two isoforms interacted differentially with different NSAIDs. Furthermore, NSAIDs were distinctly more active in inhibiting PGE2 production from endogenous AA than that from exogenous AA. These data suggest that PGE2 production through COX-2 from exogenous AA may not be subject to the same regulatory processes as that from endogenous AA and the two metabolic processes may be differentially sensitive to different NSAIDs. SN - 0952-3278 UR - https://www.unboundmedicine.com/medline/citation/9014225/Effects_of_non_steroidal_anti_inflammatory_drugs_on_prostaglandin_E2_production_by_cyclooxygenase_2_from_endogenous_and_exogenous_arachidonic_acid_in_rat_peritoneal_macrophages_stimulated_with_lipopolysaccharide_ DB - PRIME DP - Unbound Medicine ER -