Journal
ARCHIVES OF PHARMACAL RESEARCH
Volume 38, Issue 5, Pages 813-825Publisher
PHARMACEUTICAL SOC KOREA
DOI: 10.1007/s12272-014-0456-8
Keywords
4-O-methylhonokiol; Cyclooxygenase-2; Anti-inflammatory target
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Funding
- Korean government [NRF 2008-0062275, KIAT 14151 26993]
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4-O-methylhonokiol (MH) is known to inhibit inflammation by partially understood mechanisms. Here, the anti-inflammatory mechanisms of MH were examined using enzymatic, cellular, and animal assays. In enzymatic assays, MH inhibited COX-2 activity with an IC50 of 0.062 mu M, and also COX-1 with an IC50 of 2.4 mu M. In cellular assays, MH was immunotoxic above 10 mu M. At non-toxic concentrations (below 3 mu M), MH strongly inhibited COX-2-mediated prostaglandin production with an IC50 of 0.1 mu M, whereas did not or slightly affect other functions of B cells, T cells, dendritic cells, and macrophages. In an animal model, MH inhibited the increase in footpad thickness and popliteal lymph node weight in zymosan-injected mice. When analyzed the draining pLNs of zymosan-injected mice on day 5, MH inhibited the overall inflammatory responses. However, MH inhibited cyclooxygenase (COX)-2-mediated prostaglandin production without affecting tumor necrosis factor-a production in inflamed tissues within 6 h after zymosan injection. In summary, our data suggest that COX-2 may be a direct anti-inflammatory target of MH in vitro and in vivo.
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