@article {OHSHIMA2921, author = {NOBUHARU OHSHIMA and YOSHIAKI AKATSU and MASAYUKI NISHISHIRO and HIDETSUGU WAKABAYASHI and TERUO KURIHARA and KAZUE SATOH and NOBORU MOTOHASHI and KEN HASHIMOTO and HIROSHI SAKAGAMI}, title = {Inhibition of NO Production in LPS-stimulated Mouse Macrophage-like Cells by Trihaloacetylazulenes}, volume = {26}, number = {4B}, pages = {2921--2927}, year = {2006}, publisher = {International Institute of Anticancer Research}, abstract = {The effects of 26 trihaloacetylazulene derivatives on nitric oxide (NO) production by the mouse macrophage-like Raw 264.7 cells was investigated. The trichloroacetylazulenes [1b-13b] generally showed higher cytotoxicity as compared with the corresponding trifluoroacetylazulenes [1a-13a]. All the compounds inhibited NO production by lipopolysaccharide (LPS)-activated Raw 264.7 cells to various extents. 3-Trifluoroacetylguaiazulene [8a], 1-trifluoroacetyl-4,6,8-trimethylazulene [10a], 3-methyl-1-trichloroacetylazulene [2b] and 3-ethyl-1-trichloroacetylazulene [3b] showed lower cytotoxic activity and most effectively inhibited NO production. Western blot analysis revealed that compounds [8a, 10a] dose-dependently reduced the intracellular concentration of inducible NO synthase (iNOS), whereas compounds [2b, 3b] only marginally affected the iNOS protein expression. RT-PCR analysis showed that compounds [8a, 2b] reduced the iNOS mRNA expression by approximately 50\%. These compounds affected cyclooxygenase-2 protein and mRNA expression, depending on the concentrations. ESR spectroscopy revealed that compounds [8a, 10a, 2b, 3b] neither produced radical, nor scavenged NO, superoxide anion or diphenyl-2-picrylhydrazyl radicals. The present study showed the inhibitory effects of trifluoroacetylazulenes and trichloroacetylazulenes on NO production by activated macrophages. Copyright{\textcopyright} 2006 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/26/4B/2921}, eprint = {https://ar.iiarjournals.org/content/26/4B/2921.full.pdf}, journal = {Anticancer Research} }