Validation of cyclooxygenase-2 as a direct anti-inflammatory target of 4-O-methylhonokiol in zymosan-induced animal models
- Authors
- Kim, Hyung Sook; Ryu, Hwa Sun; Kim, Ji Sung; Kim, Yong Guk; Lee, Hong Kyung; Jung, Jae Kyung; Kwak, Young Shin; Lee, Kiho; Seo, Seung Yong; Yun, Jieun; Kang, Jong Soon; Hong, Jin Tae; Kim, Youngsoo; Han, Sang-Bae
- Issue Date
- May-2015
- Publisher
- PHARMACEUTICAL SOC KOREA
- Keywords
- 4-O-methylhonokiol; Cyclooxygenase-2; Anti-inflammatory target
- Citation
- ARCHIVES OF PHARMACAL RESEARCH, v.38, no.5, pp.813 - 825
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- Volume
- 38
- Number
- 5
- Start Page
- 813
- End Page
- 825
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/10564
- DOI
- 10.1007/s12272-014-0456-8
- ISSN
- 0253-6269
- Abstract
- 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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