RRC ID 67895
Author Kato Y, Kamiya H, Koide N, Odkhuu E, Komatsu T, Dagvadorj J, Watarai A, Kondo M, Kato K, Nakamura J, Yokochi T.
Title Spironolactone inhibits production of proinflammatory mediators in response to lipopolysaccharide via inactivation of nuclear factor-κB.
Journal Immunopharmacol Immunotoxicol
Abstract The effect of spironolactone (SPIR) on lipopolysaccharide (LPS)-induced production of proinflammatory mediators was examined using RAW 264.7 macrophage-like cells and mouse peritoneal macrophages. SPIR significantly inhibited LPS-induced production of nitric oxide (NO), tumor necrosis factor-α and prostaglandin E2. The inhibition was not mediated by cell death. SPIR reduced the expression of an inducible NO synthase mRNA in response to LPS. SPIR significantly inhibited phosphorylation of p65 nuclear factor (NF)-κB in response to LPS. Furthermore, SPIR inhibited phosphorylation of IκB kinase (IKK) as an upstream molecule of NF-κB in response to LPS. LPS did not induce the production of aldosterone in RAW 264.7 cells. Taken together, SPIR is suggested to inhibit LPS-induced proinflammatory mediators via inactivation of IKK/NF-κB in LPS signaling.
Volume 36(3)
Pages 237-41
Published 2014-6-1
DOI 10.3109/08923973.2014.921690
PMID 24852317
MeSH Aldosterone / biosynthesis Animals Cells, Cultured Dinoprostone / biosynthesis I-kappa B Kinase / metabolism Inflammation Mediators / antagonists & inhibitors* Inflammation Mediators / metabolism Lipopolysaccharides / pharmacology* Mice NF-kappa B / antagonists & inhibitors* Nitric Oxide / biosynthesis Phosphorylation Spironolactone / pharmacology* Tumor Necrosis Factor-alpha / biosynthesis
IF 2.352
Human and Animal Cells RAW 264(RCB0535)