RRC ID 18744
Author Nakatsuka R, Nozaki T, Shinohara M, Ohura K.
Title Dilazep decreases lipopolysaccharide-induced nitric oxide and TNF-alpha synthesis in RAW 264 cells.
Journal J Pharmacol Sci
Abstract Dilazep dihydrochloride (dilazep) is used to treat ischemic dysfunction, although the mechanisms underlying the anti-inflammatory effects of the drug have not yet been elucidated. The present study evaluated the anti-inflammatory effect of dilazep. Dilazep suppressed the production of nitric oxide (NO) and the expression of TNF-alpha mRNA by lipopolysaccharide (LPS) in RAW 264 cells. However, 1400W, an inducible NO synthase inhibitor, suppressed the production of NO but did not suppress the expression of TNF-alpha mRNA following treatment with LPS. Caffeine, an adenosine antagonist, restored LPS-stimulated NO synthesis, which is suppressed by dilazep. Therefore, these observations may suggest that the suppression of NO synthesis after dilazep treatment in RAW 264 cells is caused by the inhibition of TNF-alpha expression via adenosine receptors.
Volume 113(3)
Pages 271-5
Published 2010-1-1
DOI 10.1254/jphs.09286sc
PII JST.JSTAGE/jphs/09286SC
PMID 20647687
MeSH Animals Anti-Inflammatory Agents, Non-Steroidal / pharmacology* Cell Line, Transformed Dilazep / pharmacology* Down-Regulation / drug effects* Lipopolysaccharides / toxicity Macrophages / drug effects* Macrophages / metabolism Mice Nitric Oxide / antagonists & inhibitors Nitric Oxide / metabolism* Nitric Oxide Synthase Type II / antagonists & inhibitors Nitric Oxide Synthase Type II / genetics Nitric Oxide Synthase Type II / metabolism* Osmolar Concentration Purinergic P1 Receptor Antagonists RNA, Messenger / metabolism Receptors, Purinergic P1 / genetics Receptors, Purinergic P1 / metabolism Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha / genetics Tumor Necrosis Factor-alpha / metabolism*
IF 2.835
Times Cited 0
WOS Category PHARMACOLOGY & PHARMACY
Resource
Human and Animal Cells RAW 264(RCB0535)