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- W4313386076 abstract "Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) control inflammation through reductions in Prostaglandin E2 (PGE2) levels. Recent work by this laboratory identified NSAID-induced changes in inflammatory gene expression that appear to be independent of changes in PGE2; however, the molecular mechanism is unknown. Our goal is to determine whether NSAIDs affect gene expression via inhibition of NFkβ. Knowledge of NSAID gene control will provide a mechanism for screening novel drugs claiming anti-inflammatory properties. RAW 264.7 cells transfected with a plasmid under NFkβ control to express Secreted Alkaline Phosphatase (SEAP) were pre-treated with NSAID concentrations ranging from 10-3 to 10-7 M and stimulated with 1μg/mL LPS for 24 hours. NSAIDs from the 5 major classes inhibited SEAP release at 10-3 M, while acetylsalicylic acid (ASA) and acetaminophen did not. HEK293 cells transfected with the same plasmid were pre-treated with flunixin, diclofenac, and ASA at concentrations from 10-3 to 10-7 M and stimulated with 10ng/mL TNFα for 24 hours. Diclofenac and flunixin decreased SEAP release at 10-3 M, whereas ASA failed to inhibit SEAP release. These results demonstrate that NSAIDs prevent SEAP release via NFkβ inhibition, suggesting a new target for novel NSAIDs. Experiments to confirm NSAID inhibition of NFkβ activation by measuring the release of p65 are underway. The results of this research may also provide a screening tool for novel NSAIDs." @default.
- W4313386076 created "2023-01-06" @default.
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- W4313386076 date "2015-05-01" @default.
- W4313386076 modified "2023-09-27" @default.
- W4313386076 title "NSAIDs inhibit NFkβ activation to prevent inflammation (IRC4P.602)" @default.
- W4313386076 doi "https://doi.org/10.4049/jimmunol.194.supp.57.19" @default.
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