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Suppression of age-related inflammatory NF-κB activation by cinnamaldehyde

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Abstract

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.

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Acknowledgements

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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Correspondence to Hae Young Chung.

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Kim, D.H., Kim, C.H., Kim, MS. et al. Suppression of age-related inflammatory NF-κB activation by cinnamaldehyde. Biogerontology 8, 545–554 (2007). https://doi.org/10.1007/s10522-007-9098-2

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  • DOI: https://doi.org/10.1007/s10522-007-9098-2

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