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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on January 29, 2004; DOI: 10.1124/jpet.103.063693

0022-3565/04/3092-705-710$20.00
JPET 309:705-710, 2004
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INFLAMMATION AND IMMUNOPHARMACOLOGY

Inhibition of Nitric Oxide Generation by 23,24-Dihydrocucurbitacin D in Mouse Peritoneal Macrophages

Chang Seok Park, Hyun Lim, Kee Jung Han, Sun Heum Baek, Hyung Ok Sohn, Dong Wook Lee, Yang-Gyun Kim, Hye-Young Yun, Kwang Jin Baek, and Nyoun Soo Kwon

Department of Biochemistry, College of Medicine, Chung-Ang University, Seoul, Korea (C.S.P., H.L., K.J.H., S.H.B., Y.-G.K., H.-Y.Y., K.J.B., N.S.K.); and Laboratory of Biochemistry, KT&G Central Research Institute, Daejeon, Korea (H.O.S., D.W.L.)

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-{gamma}. DHCD decreased the levels of protein and mRNA for inducible NO synthase (iNOS). DHCD potently blocked nuclear factor-{kappa}B (NF-{kappa}B) activation, a process necessary for transcriptional activation of iNOS. These results suggested that DHCD inhibited NO generation by blocking NF-{kappa}B activation and iNOS gene transcription. Because NF-{kappa}B 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.

Received December 1, 2003; accepted January 28, 2004.

Address correspondence to: Dr. Nyoun Soo Kwon, Department of Biochemistry, College of Medicine, Chung-Ang University, 221 Heuksukdong, Dongjakgu, Seoul 156-756, Korea. E-mail: nskwon{at}cau.ac.kr




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