Dilazep Decreases Lipopolysaccharide-Induced Nitric Oxide and TNF-α Synthesis in RAW 264 Cells

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 (...

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Main Authors: Ryusuke Nakatsuka (Author), Tadashige Nozaki (Author), Mitsuko Shinohara (Author), Kiyoshi Ohura (Author)
Format: Book
Published: Elsevier, 2010-01-01T00:00:00Z.
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100 1 0 |a Ryusuke Nakatsuka  |e author 
700 1 0 |a Tadashige Nozaki  |e author 
700 1 0 |a Mitsuko Shinohara  |e author 
700 1 0 |a Kiyoshi Ohura  |e author 
245 0 0 |a Dilazep Decreases Lipopolysaccharide-Induced Nitric Oxide and TNF-α Synthesis in RAW 264 Cells 
260 |b Elsevier,   |c 2010-01-01T00:00:00Z. 
500 |a 1347-8613 
500 |a 10.1254/jphs.09286SC 
520 |a 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-α 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-α 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-α expression via adenosine receptors. Keywords:: dilazep dihydrochloride, nitric oxide, TNF-α 
546 |a EN 
690 |a Therapeutics. Pharmacology 
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786 0 |n Journal of Pharmacological Sciences, Vol 113, Iss 3, Pp 271-275 (2010) 
787 0 |n http://www.sciencedirect.com/science/article/pii/S1347861319309223 
787 0 |n https://doaj.org/toc/1347-8613 
856 4 1 |u https://doaj.org/article/fed64bc4a28c4fa2b84ccffc85b351a1  |z Connect to this object online.