Anti-inflammatory activity of (-)-aptosimon isolated from Daphne genkwa in RAW264.7 cells.

Abstract

In the present study, we investigated that (-)-aptosimon, isolated from flower buds of Daphne genkwa, inhibited cyclooxygenase-2 (COX-2) and inducible nitric oxide (NO) synthase (iNOS) expression in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Similarly, (-)-aptosimon suppressed tumor necrosis factor (TNF)-alpha production. Our results clearly indicated that (-)-aptosimon inhibited LPS-induced nuclear factor-kappaB (NF-kappaB) activation, by preventing degradation of the inhibitor kappa B-alpha (IkappaB-alpha). (-)-Aptosimon also inhibited interleukin-4 (IL-4) and interleukin-13 (IL-13) production in ConA-induced splenocytes. In conclusion, the anti-inflammatory effects of (-)-aptosimon are attributed to the suppression of pro-inflammatory cytokines and mediators by blocking NF-kappaB activation. These data suggest that (-)-aptosimon as a potential therapeutic agent for inflammation-associated disorders.

• Authors: Mee-Young Lee, Bo-Young Park, Ok-Kyoung Kwon, Ji-Eun Yuk, Sei-Ryang Oh, Hui-Seong Kim, Hyeong-Kyu Lee, Kyung-Seop Ahn
• Journal: International immunopharmacology (Int Immunopharmacol) Vol. 9 Issue 7-8 Pg. 878-85 (Jul 2009) ISSN: 1878-1705 [Electronic] Netherlands
• PMID: 19328870 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents, Non-Steroidal
• Dioxoles
• Furans
• Interleukin-13
• Lipopolysaccharides
• NF-kappa B
• Tumor Necrosis Factor-alpha
• Concanavalin A
• Interleukin-4
• aptosimon
• Nitric Oxide Synthase Type II
• Nos2 protein, mouse
• Ptgs2 protein, mouse
• Cyclooxygenase 2

Topics

• Animals
• Anti-Inflammatory Agents, Non-Steroidal (pharmacology)
• Cell Line
• Concanavalin A (metabolism)
• Cyclooxygenase 2 (genetics, metabolism)
• Daphne
• Dioxoles (pharmacology)
• Enzyme Activation (drug effects, immunology)
• Flowers
• Furans (pharmacology)
• Interleukin-13 (genetics, metabolism)
• Interleukin-4 (genetics, metabolism)
• Lipopolysaccharides (metabolism)
• Macrophages (drug effects, immunology, metabolism, pathology)
• Mice
• NF-kappa B (antagonists & inhibitors)
• Nitric Oxide Synthase Type II (genetics, metabolism)
• Phytotherapy (trends)
• Transcriptional Activation (drug effects)
• Tumor Necrosis Factor-alpha (genetics, metabolism)