Suppression of age-related inflammatory NF-κB activation by cinnamaldehyde
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Redox sensitive, pro-inflammatory nuclear transcription factor NF-κB plays a key role in both inflammation and aging processes. In a redox state disrupted by oxidative stress, pro-inflammatory genes are upregulated by the activation of NF-κB through diverse kinases. Thus, the search and characterization of new substances that modulate NF-κB are of recent research interest. Cinnamaldehyde (CNA) is the major component of cinnamon bark oil, which has been widely used as a flavoring agent in foodstuffs such as beverages and ice cream. In the present study, CNA was examined for its molecular modulation of inflammatory NF-κB activation via the redox-related NIK/IKK and MAPK pathways through the reduction of oxidative stress. Results show that age-related NF-κB activation upregulated NF-κB targeting genes, inflammatory iNOS, and COX-2, all of which were inhibited effectively by CNA. Our study further shows that CNA inhibited the activation of NF-κB via three signal transduction pathways, NIK/IKK, ERK, and p38 MAPK. Our results indicate that CNA’s antioxidative effect and the restoration of redox balance were responsible for its anti-inflammatory action. Thus, the significance of the current study is the new information revealing the anti-inflammatory properties of CNA and the role it plays in the regulation of age-related alterations in signal transduction pathways.
KeywordsNF-κB Aging Cinnamaldehyde Oxidative stress Reactive species
This work was supported by Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) through its National Nuclear Technology Program (2006-04978). We thank the Aging Tissue Bank (R21-2005-000-0008-0) funded by KOSEF and MOST for supplying the aged tissue.
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