PT  - JOURNAL ARTICLE
AU  - Chang Seok Park
AU  - Hyun Lim
AU  - Kee Jung Han
AU  - Sun Heum Baek
AU  - Hyung Ok Sohn
AU  - Dong Wook Lee
AU  - Yang-Gyun Kim
AU  - Hye-Young Yun
AU  - Kwang Jin Baek
AU  - Nyoun Soo Kwon
TI  - Inhibition of Nitric Oxide Generation by 23,24-Dihydrocucurbitacin D in Mouse Peritoneal Macrophages
AID  - 10.1124/jpet.103.063693
DP  - 2004 May 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 705--710
VI  - 309
IP  - 2
4099  - http://jpet.aspetjournals.org/content/309/2/705.short
4100  - http://jpet.aspetjournals.org/content/309/2/705.full
SO  - J Pharmacol Exp Ther2004 May 01; 309
AB  - Nitric oxide (NO) has various physiological functions. However, uncontrolled overproduction of NO can be toxic in many pathologic conditions involving inflammatory tissue damage. In the present study, we examined effects of 23,24-dihydrocucurbitacin D (DHCD) isolated from the root of Bryonia alba L. on macrophage NO generation. DHCD (<80 μM) effectively abolished NO generation from macrophages activated with lipopolysaccharide and interferon-γ. DHCD decreased the levels of protein and mRNA for inducible NO synthase (iNOS). DHCD potently blocked nuclear factor-κB (NF-κB) activation, a process necessary for transcriptional activation of iNOS. These results suggested that DHCD inhibited NO generation by blocking NF-κB activation and iNOS gene transcription. Because NF-κB activation is necessary not only for NO generation but also for many inflammatory processes, DHCD and its derivatives could be developed as anti-inflammatory drugs. The American Society for Pharmacology and Experimental Therapeutics