NDLI: The anti-inflammatory carbazole, LCY-2-CHO, inhibits lipopolysaccharide-induced inflammatory mediator expression through inhibition of the p38 mitogen-activated protein kinase signaling pathway in macrophages

Content Provider	PubMed Central
Author	Ho, Feng-ming Lai, Chih-chang Huang, Li-jiau Kuo, Tsun Cheng Chao, Chien M. Lin, Wan-wan
Copyright Year	2004
Abstract	The present study was undertaken to investigate the anti-inflammatory effects of a synthetic compound, LCY-2-CHO, on the expression of inducible nitric oxide synthase (iNOS), COX-2, and TNF-α in murine RAW264.7 macrophages. Within 1–30 μ M, LCY-2-CHO concentration-dependently inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor-α (TNF-α) formation, with IC50 values of 2.3, 1, and 0.8 μ M, respectively. Accompanying inhibition of LPS-induced iNOS, cyclooxygenase-2 (COX-2), and pro-TNF-α proteins was observed. Reverse transcription-polymerase chain reaction (RT–PCR) and promoter analyses indicated that iNOS expression was inhibited at the transcriptional level (IC50=2.3 μ M), that inhibition of COX-2 expression only partially depended on gene transcription (IC50=7.6 μ M), and that TNF-α transcription was unaffected. Transcriptional assays revealed that activation of AP-1, but not NF-κB, was concomitantly blocked by LCY-2-CHO. Our results showed that LCY-2-CHO was capable of interfering with post-transcriptional regulation, altering the stability of COX-2 and TNF-α mRNAs. Since the 3′-untranslated region (3′ UTR) of both COX-2 and TNF-α mRNA contains a p38 mitogen-activated protein kinase (MAPK)-regulated element involved in mRNA stability, we assessed the effect of LCY-2-CHO on p38 MAPK. Our data clearly indicated an inhibition (IC50=1.7 μ M) of LPS-mediated p38 MAPK activity, but not of extracellular signal-regulated kinase (ERK) or c-Jun N-terminal kinase (JNK) activity. However, kinase assays ruled out a direct inhibition of p38 MAPK action. The selective p38 MAPK inhibitor, SB203580, inhibited the promoter activities of iNOS and COX-2 rather than that of TNF-α. In conclusion, LCY-2-CHO downregulates inflammatory iNOS, COX-2, and TNF-α gene expression in macrophages through interfering with p38 MAPK and AP-1 activation.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0705700
Ending Page	1047
Page Count	11
Starting Page	1037
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	6
Volume Number	141
Language	English
Publisher Date	2004-03-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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