title: ent-kaur-16-en-19-oic Acid, isolated from the roots of Aralia continentalis, induces activation of Nrf2.
abstract: BACKGROUND
  Excessive inflammation can lead to tissue damage and dysfunction of vital organs. Hence, regulating inflammatory response is a viable therapeutic approach. In Asian countries, various inflammatory diseases have often effectively been treated with herbal remedies including the root extract of Aralia continentalis Kitagawa (Araliaceae). Here, we investigated the effect of kaurenoic acid (ent-kaur-16-en-19-oic acid: KA), a diterpenoid that is extracted from Aralia continentalis Kitagawa root, on inflammation.
  
  
  RESULTS
  Western blot and RT-PCR analyses show that KA induced the nuclear localization of Nrf2 as low as 1 nM in concentration and that KA treatment induced the expression of Nrf2 dependent genes such as GCLC and HO-1. On the other hand, KA did not affect the degradation of cytoplasmic IκB-α, the nuclear localization of RelA (p65), and NF-κB transcriptional activity in RAW264.7 cells treated with endotoxin. Consistent with these data, KA treatment failed to suppress gene expression of representative pro-inflammatory mediators including COX-2, nitric oxide, IL-1β, TNF-α, and IL-12, indicating that KA did not have an important impact on NF-κB activation.
  
  
  CONCLUSIONS
  Together, these results show that KA was an effective activator of Nrf2, and suggest that the beneficial effects of Aralia continentalis Kitagawa root extract are, at least in part, mediated by activating Nrf2.
authors: School of Korean Medicine, Pusan National University,Yangsan 626-870, Republic of Korea.
authors: Ji Hyo
authors: JH
authors: Lyu
authors: Geum San
authors: GS
authors: Lee
authors: Kyun Ha
authors: KH
authors: Kim
authors: Hyung-Woo
authors: HW
authors: Kim
authors: Su-In
authors: SI
authors: Cho
authors: Seung-Il
authors: SI
authors: Jeong
authors: Hong-Jun
authors: HJ
authors: Kim
authors: Young-Seung
authors: YS
authors: Ju
authors: Ho-Kyoung
authors: HK
authors: Kim
authors: Ruxana T
authors: RT
authors: Sadikot
authors: John W
authors: JW
authors: Christman
authors: Sei-Ryang
authors: SR
authors: Oh
authors: Hyeong-Kyu
authors: HK
authors: Lee
authors: Kyung-Seop
authors: KS
authors: Ahn
authors: Myungsoo
authors: M
authors: Joo
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology* / Q000633:toxicity; D027983:Aralia / Q000737:chemistry; D015153:Blotting, Western; D002467:Cell Nucleus / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D004224:Diterpenes / Q000302:isolation & purification / Q000494:pharmacology / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects; D057809:HEK293 Cells; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism*; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D018517:Plant Roots; D010946:Plants, Medicinal; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014162:Transfection
chemical_list: D000893:Anti-Inflammatory Agents; D004224:Diterpenes; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; C495636:Nfe2l2 protein, mouse; C014341:argyrophilic acid