RT Journal Article
SR Electronic
T1 Inhibition of Nitric Oxide Generation by 23,24-Dihydrocucurbitacin D in Mouse Peritoneal Macrophages
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 705
OP 710
DO 10.1124/jpet.103.063693
VO 309
IS 2
A1 Park, Chang Seok
A1 Lim, Hyun
A1 Han, Kee Jung
A1 Baek, Sun Heum
A1 Sohn, Hyung Ok
A1 Lee, Dong Wook
A1 Kim, Yang-Gyun
A1 Yun, Hye-Young
A1 Baek, Kwang Jin
A1 Kwon, Nyoun Soo
YR 2004
UL http://jpet.aspetjournals.org/content/309/2/705.abstract
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