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Zedoarondiol isolated from the rhizoma of Curcuma heyneana is involved in the inhibition of iNOS, COX-2 and pro-inflammatory cytokines via the downregulation of NF-κB pathway in LPS-stimulated murine macrophages

Title
Zedoarondiol isolated from the rhizoma of Curcuma heyneana is involved in the inhibition of iNOS, COX-2 and pro-inflammatory cytokines via the downregulation of NF-κB pathway in LPS-stimulated murine macrophages
Authors
Cho W.Nam J.-W.Kang H.-J.Windono T.Seo E.-K.Lee K.-T.
Ewha Authors
서은경
SCOPUS Author ID
서은경scopus
Issue Date
2009
Journal Title
International Immunopharmacology
ISSN
1567-5769JCR Link
Citation
International Immunopharmacology vol. 9, no. 9, pp. 1049 - 1057
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Several sesquiterpene lactones that have been isolated from medicinal plants are known to have many pharmacological activities. In this study, we investigated the anti-inflammatory effects of zedoarondiol, a sesquiterpene lactone isolated from the rhizoma of Curcuma heyneana, in lipopolysaccharide (LPS)-stimulated macrophage cells. Zedoarondiol dose-dependently inhibited LPS-stimulated nitric oxide (NO), prostaglandin E 2 (PGE 2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) productions in RAW 264.7 macrophage and in mouse peritoneal macrophage cells. Consistent with these findings, in RAW 264.7 cells, zedoarondiol suppressed the LPS-stimulated protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and the mRNA expressions of iNOS, COX-2, TNF-α, IL-6, and IL-1β in a concentration-dependent manner. Moreover, molecular data revealed that zedoarondiol inhibited LPS-stimulated DNA binding activity and the transcription activity of nuclear factor-kappa B (NF-κB), and this effect was accompanied by decreases in the degradation and phosphorylation of inhibitory κB (IκB)-α, and in the subsequent blocking of NF-κB translocations to the nucleus. Furthermore, zedoarondiol attenuated the phosphorylations of IκB kinase (IKK), extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (p38), and c-Jun N-terminal kinase (JNK) in LPS-stimulated RAW 264.7 cells. Taken together, the findings of the present study indicate that zedoarondiol inhibits iNOS, COX-2, and pro-inflammatory cytokine expressions by suppressing the phosphorylations of IKK and MAPKs, and by subsequently inactivating the NF-κB pathway. These relations reveal, in part, the mechanism underlying the anti-inflammatory properties of zedoarondiol. © 2009.
DOI
10.1016/j.intimp.2009.04.012
Appears in Collections:
약학대학 > 약학과 > Journal papers
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