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

• DOI: 10.1007/s10522-007-9098-2
• Publication Date: 2007-05-07T11:36:52Z
• Authors: Dae Hyun Kim; Chul Hong Kim; Min-Sun Kim; Ji Young Kim; Kyung Jin Jung; Jae Heun Chung; Won Gun An; Jae Won Lee; Byung Pal Yu; Hae Young Chung
• Keywords: Male; Aging; 0303 health sciences; Dose-Response Relationship, Drug; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Antioxidants; Rats, Inbred F344; I-kappa B Kinase; Rats; Flavoring Agents; Oxidative Stress; 03 medical and health sciences; Animals; Acrolein; Extracellular Signal-Regulated MAP Kinases; Oxidation-Reduction; Signal Transduction

Redox sensitive, pro-inflammatory nuclear transcription factor NF-kappaB 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-kappaB through diverse kinases. Thus, the search and characterization of new substances that modulate NF-kappaB 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-kappaB activation via the redox-related NIK/IKK and MAPK pathways through the reduction of oxidative stress. Results show that age-related NF-kappaB activation upregulated NF-kappaB 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-kappaB 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.